subject:(PGC 1 )

University of Alberta

1. Sutherland, Lindsey. Regulation of PGC-1 alpha in White Adipose Tissue by Exercise.

Degree: MS, Department of Agricultural, Food, and Nutritional Science, 2009, University of Alberta

URL: https://era.library.ualberta.ca/files/vq27zp66j

► This project investigated the effects of exercise and epinephrine on the mRNA expression of peroxisome proliferator activated receptor gamma coactivator-1 alpha (PGC-1 alpha), a master… (more)

Subjects/Keywords: mitochondria; adipose; PGC-1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sutherland, L. (2009). Regulation of PGC-1 alpha in White Adipose Tissue by Exercise. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/vq27zp66j

Chicago Manual of Style (16^th Edition):

Sutherland, Lindsey. “Regulation of PGC-1 alpha in White Adipose Tissue by Exercise.” 2009. Masters Thesis, University of Alberta. Accessed January 22, 2021. https://era.library.ualberta.ca/files/vq27zp66j.

MLA Handbook (7^th Edition):

Sutherland, Lindsey. “Regulation of PGC-1 alpha in White Adipose Tissue by Exercise.” 2009. Web. 22 Jan 2021.

Vancouver:

Sutherland L. Regulation of PGC-1 alpha in White Adipose Tissue by Exercise. [Internet] [Masters thesis]. University of Alberta; 2009. [cited 2021 Jan 22]. Available from: https://era.library.ualberta.ca/files/vq27zp66j.

Council of Science Editors:

Sutherland L. Regulation of PGC-1 alpha in White Adipose Tissue by Exercise. [Masters Thesis]. University of Alberta; 2009. Available from: https://era.library.ualberta.ca/files/vq27zp66j

2. Fogarty, Stuart A. SMURF1 as a Novel Regulator of PGC-1a.

Degree: Biological Sciences - Cell and Molecular: M.S., Biology, 2016, St. Cloud State University

URL: https://repository.stcloudstate.edu/biol_etds/9

► Parkinson’s disease is a neurodegenerative disorder caused by the impairment and/or death of the dopaminergic neurons in the area of the brain that controls… (more)

Subjects/Keywords: SMURF1 CRISPR siRNA PGC-1 Parkinson's Regulator

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fogarty, S. A. (2016). SMURF1 as a Novel Regulator of PGC-1a. (Masters Thesis). St. Cloud State University. Retrieved from https://repository.stcloudstate.edu/biol_etds/9

Chicago Manual of Style (16^th Edition):

Fogarty, Stuart A. “SMURF1 as a Novel Regulator of PGC-1a.” 2016. Masters Thesis, St. Cloud State University. Accessed January 22, 2021. https://repository.stcloudstate.edu/biol_etds/9.

MLA Handbook (7^th Edition):

Fogarty, Stuart A. “SMURF1 as a Novel Regulator of PGC-1a.” 2016. Web. 22 Jan 2021.

Vancouver:

Fogarty SA. SMURF1 as a Novel Regulator of PGC-1a. [Internet] [Masters thesis]. St. Cloud State University; 2016. [cited 2021 Jan 22]. Available from: https://repository.stcloudstate.edu/biol_etds/9.

Council of Science Editors:

Fogarty SA. SMURF1 as a Novel Regulator of PGC-1a. [Masters Thesis]. St. Cloud State University; 2016. Available from: https://repository.stcloudstate.edu/biol_etds/9

Université de Sherbrooke

3. Thériault, Mathieu. Étude de l'interaction de ERR[alpha] et de ses corégulateurs dans le carcinome colorectal.

Degree: 2012, Université de Sherbrooke

URL: http://hdl.handle.net/11143/6364

► Le récepteur relié au récepteur à l'estrogène alpha (ERR?) est un récepteur orphelin de la superfamille des récepteurs nucléaires impliqué dans la régulation du métabolisme… (more)

▼ Le récepteur relié au récepteur à l'estrogène alpha (ERR?) est un récepteur orphelin de la superfamille des récepteurs nucléaires impliqué dans la régulation du métabolisme énergétique. II cause l'expression de gènes impliqués dans les différentes voies métaboliques et peut ainsi augmenter le potentiel de production d'énergie des cellules. Fidèle à son état d'orphelin, l'activité de ERR? ne semble pas être régulée via la liaison d'un ligand, mais plutôt via la présence des corégulateurs. Les corégulateurs sont des protéines ayant pour fonction d'assister ou de nuire à l'action des récepteurs nucléaires et autres facteurs de transcription dans l'expression de leurs gènes cibles. L'étude de l'interaction entre ERR? et ses corégulateurs s'avère donc être incontournable pour la compréhension de son rôle dans les divers processus où il est impliqué et dans les pathologies auxquelles il est associé comme le cancer qui est un dérèglement cellulaire causé par des altérations génétiques, et est caractérisé par une prolifération incontrôlée de cellules au sein d'un organisme. Pour qu'une cellule devienne cancéreuse, elle doit acquérir des mutations précises au niveau du génome causant des modifications dans la régulation de différents processus. Un de ces processus est le métabolisme énergétique. Le but de ma maîtrise était d'identifier et d'étudier les corégulateurs de ERR? (PGC-1?, PGC-1? et PRC) et leur modulation de gènes cibles de ERR? dans le contexte du métabolisme énergétique du cancer. L'expression de ERR? et des trois membres de la famille PGC-1 a été mesurée par qPCR sur des tissus colorectaux sains et cancéreux appropriés. L'expression de ERR? ne semble pas significativement différente suivant l'apparition de la pathologie, alors que l'expression des coactivateurs PGC1-? et PGC-1? s'avère moins élevée dans les tissus cancéreux par rapport aux tissus sains. L'expression de PRC est plus grande dans le cancer colorectal. Ces résultats suggèrent que PRC pourrait posséder un rôle, exclusif à sa famille, dans le carcinome colorectal. Afin de trouver de nouveaux corégulateurs de ERR?, nous avons procédé à une expérience de double hybride sur levure qui a permis d'identifier 6 nouveaux partenaires d'interactions du récepteur : La leucine aminopeptidase 3 (LAP3), le synaptic nuclear envelope protein 1 (SYNE1 /nesprinl ), le proteasome macropain 26S subunit ATPase (PSMC5), la DEAD box polypeptide 1 (DDXI), le ring finger protein 2 (RNF2/Ring2) et l'interferon-related developmental regulator IFRD1. Leurs fonctions connues peuvent toutes être associées à l'action de ERR?, soit en régulant sa dégradation ou son activité. En particulier, nos résultats pour 1FRD1 montrent que son expression est supérieure dans la presque totalité des cancers colorectaux étudiés par rapport aux tissus sains adjacents. On peut ainsi supposer que cette protéine possède une fonction encourageant la carcinogenèse. De plus, des essais luciférases ont montré qu'IFRD1 augmente l'activité du récepteur nucléaire ERR?. Le partenariat entre ERR? et IFRD I… Advisors/Committee Members: Carrier, Julie (advisor).

Subjects/Keywords: IFRD1; PRC; PGC-1; ERR[alpha]

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Thériault, M. (2012). Étude de l'interaction de ERR[alpha] et de ses corégulateurs dans le carcinome colorectal. (Masters Thesis). Université de Sherbrooke. Retrieved from http://hdl.handle.net/11143/6364

Chicago Manual of Style (16^th Edition):

Thériault, Mathieu. “Étude de l'interaction de ERR[alpha] et de ses corégulateurs dans le carcinome colorectal.” 2012. Masters Thesis, Université de Sherbrooke. Accessed January 22, 2021. http://hdl.handle.net/11143/6364.

MLA Handbook (7^th Edition):

Thériault, Mathieu. “Étude de l'interaction de ERR[alpha] et de ses corégulateurs dans le carcinome colorectal.” 2012. Web. 22 Jan 2021.

Vancouver:

Thériault M. Étude de l'interaction de ERR[alpha] et de ses corégulateurs dans le carcinome colorectal. [Internet] [Masters thesis]. Université de Sherbrooke; 2012. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/11143/6364.

Council of Science Editors:

Thériault M. Étude de l'interaction de ERR[alpha] et de ses corégulateurs dans le carcinome colorectal. [Masters Thesis]. Université de Sherbrooke; 2012. Available from: http://hdl.handle.net/11143/6364

4. Llimona, Flávia. Co-ativador de transcrição gênica PGC-1 na pancreatite aguda.

Degree: PhD, Processos Inflamatórios e Alérgicos, 2011, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5165/tde-20052011-174649/ ;

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PGC-1 é uma família de coativadores de fatores de transcrição que controlam a expressão de diversos genes envolvidos na homeostase energética celular. As isoformas PGC-1… (more)

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PGC-1 é uma família de coativadores de fatores de transcrição que controlam a expressão de diversos genes envolvidos na homeostase energética celular. As isoformas PGC-1 e estão presente em tecidos com alto metabolismo oxidativo e são capazes de aumentar biogênese mitocondrial, -oxidação de ácidos graxos e gliconeogênese em resposta à exposição ao frio, jejum e exercício. Inicialmente mostramos que macrófagos in vitro aumentaram a expressão de PGC-1 após 1h da exposição à zymosan. Com isso, hipotetizamos que PGC-1 poderia ter sua expressão aumentada em resposta a um insulto bacteriano. Para verificar nossa hipótese analisamos a expressão de PGC-1 em um modelo de pancreatite aguda (PA), caracterizada por uma forte resposta inflamatória estéril inicial, seguida, após poucos dias, por translocação bacteriana intestinal e infecção disseminada. PA foi induzida por infusão retrograda de taurocolato de sódio (2,5%). Também analisamos PGC-1 em um modelo de sepse por ligadura e perfuração cecal (CLP), cujo conteúdo intestinal é depositado no peritôneo, causando infecção grave local e disseminada. Animais tratados com Imipenem durante 48h após PA também foram analisados, bem como a interferência de PGC-1 ASO no processo de fagocitose. A expressão de PGC-1 e foi medida por PCR quantitativo. PA foi confirmada pelo aumento da amilase sérica e a inflamação sistêmica ratificada por leucocitose. PGC1 aumentou no baço e nos leucócitos circulantes 48h após PA e no lavado peritoneal 24h após PA e CLP. No entanto, PGC1 diminuiu no baço 24h após PA. Tratamento com Imipenem diminuiu PGC- 1. A diminuição de PGC-1 após transfecção com ASO levou à redução do processo de fagocitose. Assim, concluímos que ocorre aumento de PGC-1 na presença de bactérias e esse aumento está relacionado com fagocitose

PGC1 is a family of transcriptional coactivators that controls the expression of several genes involved in cell energy homeostasis. PGC1 isoforms and are present in tissues with high oxidative metabolism and are able to enhance mitochondrial biogenesis, -oxidation of fatty acids and gluconeogenesis in response to exposure to cold, fasting and exercise. Initial results showed macrophages in vitro present increased PGC-1 expression after 1h exposure to zymosan. Thus, we hypothesized that PGC-1 could be up-regulated in response to bacterial insult. We tested our hypothesis following PGC-1 expression in an acute pancreatitis (AP) model, characterized initially by a strong sterile inflammatory response, followed, few days later, by bacterial intestinal translocation and disseminated infection. AP was induced by retrograde infusion of sodium taurocholate (2.5%). We also analysed PGC-1 in a model of sepsis by cecal ligation and puncture (CLP), whose intestinal content is deposited in the peritoneum, causing a severe local and disseminated infection. Animals submitted to PA and treated with Imipenem for 48 hours were also analyzed, as well as the interference of PGC-1 ASO in phagocytosis process. PGC-1 and expression were measured by quantitative…

Advisors/Committee Members: Souza, Heraldo Possolo de.

Subjects/Keywords: Bacterial translocation; Fagocitose; Pancreatite; Pancreatitis; PGC-1; PGC-1; Phagocytosis; Sepse; Sepsis; Translocação bacteriana

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APA (6^th Edition):

Llimona, F. (2011). Co-ativador de transcrição gênica PGC-1 na pancreatite aguda. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5165/tde-20052011-174649/ ;

Chicago Manual of Style (16^th Edition):

Llimona, Flávia. “Co-ativador de transcrição gênica PGC-1 na pancreatite aguda.” 2011. Doctoral Dissertation, University of São Paulo. Accessed January 22, 2021. http://www.teses.usp.br/teses/disponiveis/5/5165/tde-20052011-174649/ ;.

MLA Handbook (7^th Edition):

Llimona, Flávia. “Co-ativador de transcrição gênica PGC-1 na pancreatite aguda.” 2011. Web. 22 Jan 2021.

Vancouver:

Llimona F. Co-ativador de transcrição gênica PGC-1 na pancreatite aguda. [Internet] [Doctoral dissertation]. University of São Paulo; 2011. [cited 2021 Jan 22]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5165/tde-20052011-174649/ ;.

Council of Science Editors:

Llimona F. Co-ativador de transcrição gênica PGC-1 na pancreatite aguda. [Doctoral Dissertation]. University of São Paulo; 2011. Available from: http://www.teses.usp.br/teses/disponiveis/5/5165/tde-20052011-174649/ ;

5. Passos, Luis Augusto Abreu da Cunha. A sinalização do co-ativador de transcrição PGC-1beta e sua relevância para a proliferação celular e desenvolvimento de melanoma.

Degree: PhD, Processos Inflamatórios e Alérgicos, 2015, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5165/tde-31032015-162021/ ;

►

PGC-1 beta é um co-ativador de transcrição gênica responsável pela regulação do metabolismo celular, principalmente na biogênese e função mitocondrial, disponibilidade de substrato e síntese… (more)

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PGC-1 beta é um co-ativador de transcrição gênica responsável pela regulação do metabolismo celular, principalmente na biogênese e função mitocondrial, disponibilidade de substrato e síntese de lipídios. Nos últimos anos, outras isoformas de PGC-1 têm sido descritos como participantes na gênese e manutenção de tumores. Portanto, nosso objetivo foi determinar se o PGC-1beta está relacionado ao aumento da proliferação celular de células de melanoma. Inicialmente, foi demonstrado que os níveis de RNAm e proteína de PGC-1beta são muito mais elevados em linhagens de células de melanoma (Tm1 e Tm5) do que na linhagem parental de melanócitos não tumorais (Melan-a) como detectado por PCR quantitativa e western blotting. A fim de descobrir uma relação causal entre a expressão de PGC-1? e crescimento celular da linhagem Tm5, células de tal linhagem foram transfectadas com um oligonucleotídeo antisense (ASO) contra PGC-1beta. As células tratados com ASO apresentaram níveis mais baixos de RNAm e proteína PGC-1beta, além de redução em sua atividade avaliada pela expressão de genes PGC-1beta dependentes. Além disso, as células transfectadas apresentaram uma taxa de proliferação inferior em comparação com células de controle Tm5. Este fenômeno também foi observado in vivo. Quando injetadas em camundongos, as células Tm5 desenvolvem-se em um tumor que atinge 1,34 ± 0,20 cm3 após nove dias. Tumores tratados com ASO após o mesmo tempo apresentaram volume tumoral de 0,75 ± 0,05 cm3. Este crescimento não estava relacionada à necrose tumoral, mas sim com a proliferação reduzida de células. Finalmente, verificamos se o mesmo fenômeno seria observado em humanos. A expressão PGC-1beta foi muito maior em amostras de melanoma do que em nevos, alterações não-malignas da pele com alto conteúdo de melanina. Por conseguinte, conclui-se que a expressão PGC-1? está aumentada no melanoma, tanto murino e humano, e que o bloqueio da sua atividade leva à diminuição da proliferação celular e crescimento tumoral

PGC-1beta is a co-activator of gene transcription primarily responsible for the regulation of cellular metabolism, mainly in mitochondrial biogenesis and function and also substrate and lipid synthesis. In recent years, other isoforms of PGC-1 have been described as participating in the genesis and maintenance of tumors. Therefore, our objective was to determine whether PGC-1beta is related to increased proliferation of melanoma cells. Initially, it was demonstrated that mRNA and protein levels of PGC-1beta are much higher in melanoma cell lines (Tm1 and TM5) than in the non-tumoral parental lineage melanocytes (melan-a) as detected by quantitative PCR and Western blotting. In order to find a causal relationship between the expression of PGC-1beta and cell growth, Tm5 lineage cells were transfected with an antisense oligonucleotide (ASO) against PGC-1beta. The cells treated with ASO had lower levels of PGC-1beta mRNA and protein, as well as reduction in its activity detected by quantitation of PGC-1beta dependent genes expression.…

Advisors/Committee Members: Souza, Heraldo Possolo de.

Subjects/Keywords: Cell proliferation; Cutaneous neoplasias; Melanoma; Melanoma; Neoplasias cutâneas; PGC-1; PGC-1beta; Proliferação de células

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Passos, L. A. A. d. C. (2015). A sinalização do co-ativador de transcrição PGC-1beta e sua relevância para a proliferação celular e desenvolvimento de melanoma. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5165/tde-31032015-162021/ ;

Chicago Manual of Style (16^th Edition):

Passos, Luis Augusto Abreu da Cunha. “A sinalização do co-ativador de transcrição PGC-1beta e sua relevância para a proliferação celular e desenvolvimento de melanoma.” 2015. Doctoral Dissertation, University of São Paulo. Accessed January 22, 2021. http://www.teses.usp.br/teses/disponiveis/5/5165/tde-31032015-162021/ ;.

MLA Handbook (7^th Edition):

Passos, Luis Augusto Abreu da Cunha. “A sinalização do co-ativador de transcrição PGC-1beta e sua relevância para a proliferação celular e desenvolvimento de melanoma.” 2015. Web. 22 Jan 2021.

Vancouver:

Passos LAAdC. A sinalização do co-ativador de transcrição PGC-1beta e sua relevância para a proliferação celular e desenvolvimento de melanoma. [Internet] [Doctoral dissertation]. University of São Paulo; 2015. [cited 2021 Jan 22]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5165/tde-31032015-162021/ ;.

Council of Science Editors:

Passos LAAdC. A sinalização do co-ativador de transcrição PGC-1beta e sua relevância para a proliferação celular e desenvolvimento de melanoma. [Doctoral Dissertation]. University of São Paulo; 2015. Available from: http://www.teses.usp.br/teses/disponiveis/5/5165/tde-31032015-162021/ ;

6. Mazzucatto, Flávio. Potencial do treinamento físico para a prevenção de distúrbios metabólicos induzidos por dieta hipercalórica.

Degree: Mestrado, Biodinâmica do Movimento Humano, 2013, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/39/39132/tde-06082013-135619/ ;

►

O aumento do consumo de alimentos ricos em gorduras e carboidratos associado à reduzida prática de exercícios físicos pode ter como consequência o desenvolvimento da… (more)

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O aumento do consumo de alimentos ricos em gorduras e carboidratos associado à reduzida prática de exercícios físicos pode ter como consequência o desenvolvimento da obesidade e de distúrbios metabólicos, tais como intolerância à glicose, resistência à insulina, diabetes tipo 2 e dislipidemias. O músculo esquelético contribui diretamente para o desenvolvimento e progressão dos distúrbios metabólicos, especialmente em decorrência da disfunção mitocondrial. Uma das ferramentas amplamente utilizada para o tratamento de distúrbios metabólicos é o treinamento físico, pois promove adaptações metabólicas no sentido oposto aos prejuízos metabólicos induzidos por dietas hipercalóricas. O presente estudo teve por objetivo avaliar se o treinamento físico aeróbio seria capaz de prevenir o desenvolvimento de distúrbios metabólicos induzidos por dieta hipercalórica composta por ração de cafeteria mais frutose e sacarose diluídas em água de beber em camundongos, e se essa resposta seria mediada por adaptações no músculo esquelético. Os resultados obtidos revelaram que o treinamento físico aeróbio preveniu os distúrbios metabólicos induzidos por dieta hipercalórica, tais como deposição de gordura, hiperfagia, hiperglicemia e aumento de pressão arterial, bem como melhorou a capacidade aeróbia. Essas respostas foram associadas apenas ao aumento na capilarização do músculo esquelético, já que a capacidade oxidativa determinada pela citrato sintase e a expressão da proteína PGC-1? não modificaram

The increased consumption of foods rich in fats and carbohydrates associated with reduced physical exercise may result in the development of obesity and metabolic disorders such as glucose intolerance, insulin resistance, type 2 diabetes and dyslipidemia. Skeletal muscle contributes directly to the development and progression of metabolic disorders, especially as a result of mitochondrial dysfunction. One of the tools widely used for the treatment of metabolic disorders is physical training, which promotes metabolic adaptations in the opposite direction to metabolic damage induced by hypercaloric diets. The present study aimed to evaluate whether physical training could prevent the development of metabolic disorders induced by hypercaloric diet consisting of cafeteria diet plus fructose and sucrose diluted in drinking water in mice, and if this response was mediated by adaptations in skeletal muscle. The results showed that physical training prevented metabolic disorders induced by hypercaloric diet, such as fat deposition, hyperphagia, hyperglycemia, increased blood pressure, and improved aerobic capacity. These responses were associated only with the increase in skeletal muscle capillarity, because oxidative capacity citrate synthase and protein expression of PGC-1? did not change

Advisors/Committee Members: Evangelista, Fabiana de Sant\'Anna.

Subjects/Keywords: Capilarização; Capillarity; Dieta hipercalórica; Glicemia; Glycemia; Hypercaloric diet; PGC-1?; PGC-1?; Physical training; Treinamento físico

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mazzucatto, F. (2013). Potencial do treinamento físico para a prevenção de distúrbios metabólicos induzidos por dieta hipercalórica. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/39/39132/tde-06082013-135619/ ;

Chicago Manual of Style (16^th Edition):

Mazzucatto, Flávio. “Potencial do treinamento físico para a prevenção de distúrbios metabólicos induzidos por dieta hipercalórica.” 2013. Masters Thesis, University of São Paulo. Accessed January 22, 2021. http://www.teses.usp.br/teses/disponiveis/39/39132/tde-06082013-135619/ ;.

MLA Handbook (7^th Edition):

Mazzucatto, Flávio. “Potencial do treinamento físico para a prevenção de distúrbios metabólicos induzidos por dieta hipercalórica.” 2013. Web. 22 Jan 2021.

Vancouver:

Mazzucatto F. Potencial do treinamento físico para a prevenção de distúrbios metabólicos induzidos por dieta hipercalórica. [Internet] [Masters thesis]. University of São Paulo; 2013. [cited 2021 Jan 22]. Available from: http://www.teses.usp.br/teses/disponiveis/39/39132/tde-06082013-135619/ ;.

Council of Science Editors:

Mazzucatto F. Potencial do treinamento físico para a prevenção de distúrbios metabólicos induzidos por dieta hipercalórica. [Masters Thesis]. University of São Paulo; 2013. Available from: http://www.teses.usp.br/teses/disponiveis/39/39132/tde-06082013-135619/ ;

7. 小山, 淑正. Uncoupling of peripheral and master clock gene rhythms by reversed feeding leads to an exacerbated inflammatory response after polymicrobial sepsis in mice.

Degree: 博士(医学), 2016, Oita University / 大分大学

URL: http://hdl.handle.net/10559/15608

► Reversed feeding uncouples peripheral and master clock gene rhythms and leads to an increased risk of disease development. The aim of this study was to… (more)

Subjects/Keywords: sepsis; sirtuin-1; PGC-1α; pro-inflammatory cytokines; survival rate

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

小山, �. (2016). Uncoupling of peripheral and master clock gene rhythms by reversed feeding leads to an exacerbated inflammatory response after polymicrobial sepsis in mice. (Thesis). Oita University / 大分大学. Retrieved from http://hdl.handle.net/10559/15608

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

小山, 淑正. “Uncoupling of peripheral and master clock gene rhythms by reversed feeding leads to an exacerbated inflammatory response after polymicrobial sepsis in mice.” 2016. Thesis, Oita University / 大分大学. Accessed January 22, 2021. http://hdl.handle.net/10559/15608.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

小山, 淑正. “Uncoupling of peripheral and master clock gene rhythms by reversed feeding leads to an exacerbated inflammatory response after polymicrobial sepsis in mice.” 2016. Web. 22 Jan 2021.

Vancouver:

小山 �. Uncoupling of peripheral and master clock gene rhythms by reversed feeding leads to an exacerbated inflammatory response after polymicrobial sepsis in mice. [Internet] [Thesis]. Oita University / 大分大学; 2016. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10559/15608.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

小山 �. Uncoupling of peripheral and master clock gene rhythms by reversed feeding leads to an exacerbated inflammatory response after polymicrobial sepsis in mice. [Thesis]. Oita University / 大分大学; 2016. Available from: http://hdl.handle.net/10559/15608

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

UCLA

8. O'Donnell, Kelley. Mitochondrial Transport and Function in Axon Degeneration.

Degree: Neuroscience, 2013, UCLA

URL: http://www.escholarship.org/uc/item/0q20j9bg

► Axon degeneration plays a critical but ill-defined role in Parkinson disease (PD), and is actively regulated by pathways that are not well understood. Mitochondria orchestrate… (more)

▼ Axon degeneration plays a critical but ill-defined role in Parkinson disease (PD), and is actively regulated by pathways that are not well understood. Mitochondria orchestrate many of the processes that underlie axonal homeostasis, and mitochondrial dysfunction is implicated in PD pathogenesis. A better understanding of axonal mitochondria may therefore identify the cell biological processes that mediate degeneration and protection of the axon. Recent studies have suggested that mitochondrial transport is critical to axon protection after injury. I studied mitochondrial morphology, transport, and function in living zebrafish embryos. Using time-lapse confocal imaging of peripheral sensory neurons, I investigated the effect of injury on mitochondrial transport. I used two-photon laser axotomy to induce Wallerian degeneration (WD) of the distal axon. I found that acute transport arrest occurs in the distal axon, and motility does not recover before fragmentation. Although transport arrest was preserved in the proximal axon, which does not degenerate, increased mitochondrial trafficking after injury did not always correlate with axon protection. To determine whether mitochondrial ROS production is relevant to WD, I expressed the redox-sensitive biosensor roGFP2 in the mitochondrial matrix. After injury, roGFP2 was rapidly and persistently oxidized in the distal, but not the proximal, axon. The axon-protective protein WldS, which had only a mild and temporary effect on transport arrest after axotomy, robustly inhibited roGFP2 oxidation and degeneration. To further investigate the importance of mitochondrial ROS production after injury, I expressed the transcriptional co-activator PGC-1alpha, which has roles in mitochondrial biogenesis and ROS detoxification. I saw that overexpression of this protein delays roGFP2 oxidation after injury, and delays WD. Mitochondrial ROS production is therefore a better predictor of axonal vulnerability than mitochondrial transport, and ROS detoxification may be a relevant therapeutic target to prevent axon degeneration. I then studied degeneration induced by alpha-synuclein (aSyn), a protein that is associated with PD. I expressed human wild-type aSyn in peripheral sensory neurons and saw that axon pathology precedes cell death in these cells. Early changes in mitochondrial morphology were consistent with increased fragmentation, and axonal varicosities were filled with swollen mitochondria. I also saw reduced mitochondrial trafficking in aSyn-expressing cells. Motile mitochondria favored retrograde transport towards the cell body. I hypothesized that protection of mitochondria might prevent degeneration in this model, as it had after axotomy. I therefore expressed PGC-1alpha in cells expressing aSyn, and saw robust protection against axon degeneration and cell death. These results suggest that axon degeneration pathways converge on mitochondrial dysfunction. Protection of mitochondria may therefore be a promising therapeutic target in the prevention and treatment of neurodegenerative…

Subjects/Keywords: Neurosciences; alpha-synuclein; axon degeneration; mitochondria; Parkinson disease; PGC-1; zebrafish

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

O'Donnell, K. (2013). Mitochondrial Transport and Function in Axon Degeneration. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/0q20j9bg

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

O'Donnell, Kelley. “Mitochondrial Transport and Function in Axon Degeneration.” 2013. Thesis, UCLA. Accessed January 22, 2021. http://www.escholarship.org/uc/item/0q20j9bg.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

O'Donnell, Kelley. “Mitochondrial Transport and Function in Axon Degeneration.” 2013. Web. 22 Jan 2021.

Vancouver:

O'Donnell K. Mitochondrial Transport and Function in Axon Degeneration. [Internet] [Thesis]. UCLA; 2013. [cited 2021 Jan 22]. Available from: http://www.escholarship.org/uc/item/0q20j9bg.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

O'Donnell K. Mitochondrial Transport and Function in Axon Degeneration. [Thesis]. UCLA; 2013. Available from: http://www.escholarship.org/uc/item/0q20j9bg

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Université de Lorraine

9. Mimoun, Khalid. Effets de la carence en vitamine B12 au niveau cérébral chez le modèle murin invalidé pour le gène CD320 : approche comportementale et mécanismes moléculaires de l'apprentissage hippocampo-dépendant : Effects of vitamine B12 deficiency on the brain in the murine model invalidated for the CD 320 gene : Behavioral approch and molecular mechanisms of hippocampo-dependent learning.

Degree: Docteur es, Sciences de la vie et de la santé, 2017, Université de Lorraine

URL: http://www.theses.fr/2017LORR0262

►

Il est maintenant clairement établi que la vitamine B12 (cobalamine) joue un rôle important dans la formation des globules rouges, et joue un rôle essentiel… (more)

▼

Il est maintenant clairement établi que la vitamine B12 (cobalamine) joue un rôle important dans la formation des globules rouges, et joue un rôle essentiel dans l'efficacité du fonctionnement du système nerveux, comme les fonctions cognitives. La carence en vitamine B12 est répandue dans le monde et provoque une anémie mégaloblastique et des déficits neurologiques. La carence en vitamine B12 et l'hyperactivité glucocorticoïde (GC) contribuent à la détérioration de la plasticité et des fonctions de l'hippocampe. Pour comprendre comment la carence en cobalamine dans le système nerveux central génère des déficits neurologiques fonctionnels, nous avons utilisé un modèle de souris génétiquement modifiées, dont le gène codant le récepteur de la transcobalamine (souris CD320 KO) est invalidé exclusivement dans le cerveau. Nos analyses comportementales indiquent des déficits dans l'apprentissage visuo-spatial hippocampo-dépendant chez les souris KO. Les résultats ont montré qu'une dose journalière physiologique d'hydroxycortisone (8 mg / kg / jour I.P.) a un effet positif dans la restauration dans les performances d'apprentissage, chez les souris KO par rapport aux contrôles. Conformément aux déficits comportementaux, ce modèle knock-out montre une diminution de l'expression de protéines clés impliquées dans la plasticité cérébrale. Les résultats de western blot des extraits d'hippocampe ont révélé que les souris KO femelles montrent une diminution de l'expression des récepteurs des glucocorticoïdes (GR) et du coactivateur Proliférateur de péroxysome 1 (PGC-1), la protéine de réponse de croissance précoce -1 (EGR-1), Synapsines (Syn I, II), protéines clés connues pour être impliquées dans l'activité synaptique. L'étude du modèle CD320 KO pourrait permettre de mieux comprendre les effets de la carence en vitamine B12 observés chez l'homme, afin d’identifier des réponses potentielles aux différents troubles neurologiques associés ; notamment peut être un traitement palliatif basé sur les corticoïdes

It is now clearly established that vitamin B12 (or cobalamin), plays an important role in the formation of red blood cells, as well as it has a vital role in the efficient functioning of the nervous system such as cognitive functions. Vitamin B12 deficiency is widespread worldwide and causes megaloblastic anemia and neurological deficits. Vitamin B12 deficiency and the hyperactivity of the glucocorticoid (GC) contribute to the deterioration of hippocampal plasticity and functions. To understand whether cobalamin deficiency in the central nervous system produced functional neurologic deficits, we used a transcobalamin receptor / CD320 knockout mouse that lacks the receptor for the cellular uptake of cobalamin in the brain. Our behavioral analyses indicate deficits in hippocampo-dependant visuo-spatial learning capacities in KO mice. However, a daily physiological dose of hydroxycortisone (8 mg/kg/day I.P.) has a positive effect in improving learning performances in KO mice compared to controls. Consistent with the behavioral…

Advisors/Committee Members: Pourié, Grégory (thesis director), Dreumont, Natacha (thesis director).

Subjects/Keywords: Cobalamine; Souris CD 320 knockout; Glucocorticoïdes; PGC-1; Synapsine; Plasticité synaptique; Cobalamin; Glucocorticoids; CD320 knockout mouse; PGC-1; Synapsines; Synaptic plasticity; 612.399; 573.86

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APA (6^th Edition):

Mimoun, K. (2017). Effets de la carence en vitamine B12 au niveau cérébral chez le modèle murin invalidé pour le gène CD320 : approche comportementale et mécanismes moléculaires de l'apprentissage hippocampo-dépendant : Effects of vitamine B12 deficiency on the brain in the murine model invalidated for the CD 320 gene : Behavioral approch and molecular mechanisms of hippocampo-dependent learning. (Doctoral Dissertation). Université de Lorraine. Retrieved from http://www.theses.fr/2017LORR0262

Chicago Manual of Style (16^th Edition):

Mimoun, Khalid. “Effets de la carence en vitamine B12 au niveau cérébral chez le modèle murin invalidé pour le gène CD320 : approche comportementale et mécanismes moléculaires de l'apprentissage hippocampo-dépendant : Effects of vitamine B12 deficiency on the brain in the murine model invalidated for the CD 320 gene : Behavioral approch and molecular mechanisms of hippocampo-dependent learning.” 2017. Doctoral Dissertation, Université de Lorraine. Accessed January 22, 2021. http://www.theses.fr/2017LORR0262.

MLA Handbook (7^th Edition):

Mimoun, Khalid. “Effets de la carence en vitamine B12 au niveau cérébral chez le modèle murin invalidé pour le gène CD320 : approche comportementale et mécanismes moléculaires de l'apprentissage hippocampo-dépendant : Effects of vitamine B12 deficiency on the brain in the murine model invalidated for the CD 320 gene : Behavioral approch and molecular mechanisms of hippocampo-dependent learning.” 2017. Web. 22 Jan 2021.

Vancouver:

Mimoun K. Effets de la carence en vitamine B12 au niveau cérébral chez le modèle murin invalidé pour le gène CD320 : approche comportementale et mécanismes moléculaires de l'apprentissage hippocampo-dépendant : Effects of vitamine B12 deficiency on the brain in the murine model invalidated for the CD 320 gene : Behavioral approch and molecular mechanisms of hippocampo-dependent learning. [Internet] [Doctoral dissertation]. Université de Lorraine; 2017. [cited 2021 Jan 22]. Available from: http://www.theses.fr/2017LORR0262.

Council of Science Editors:

Mimoun K. Effets de la carence en vitamine B12 au niveau cérébral chez le modèle murin invalidé pour le gène CD320 : approche comportementale et mécanismes moléculaires de l'apprentissage hippocampo-dépendant : Effects of vitamine B12 deficiency on the brain in the murine model invalidated for the CD 320 gene : Behavioral approch and molecular mechanisms of hippocampo-dependent learning. [Doctoral Dissertation]. Université de Lorraine; 2017. Available from: http://www.theses.fr/2017LORR0262

Queens University

10. Bremer, Katharina. Environmental Sensitivity of Mitochondrial Gene Expression in Fish .

Degree: Biology, 2013, Queens University

URL: http://hdl.handle.net/1974/8433

► Maintaining energy organismal homeostasis under changing physiological and environmental conditions is vital, and requires constant adjustments of the energy metabolism. Central to meeting energy demands… (more)

▼ Maintaining energy organismal homeostasis under changing physiological and environmental conditions is vital, and requires constant adjustments of the energy metabolism. Central to meeting energy demands is the regulation of mitochondrial oxidative capacity. When demands increase, animals can increase mitochondrial content/enzymes, known as mitochondrial biogenesis. Central to mammalian mitochondrial biogenesis is the transcriptional master regulator PPARγ (peroxisome proliferator-activated receptor γ) coactivator-1α (PGC-1α), and the network of DNA-binding proteins it coactivates (e.g. nuclear respiratory factor 1 and 2 [NRF-1, NRF-2], estrogen-related receptor α [ERRα], thyroid receptor α [TRα-1], retinoid X receptor α [RXRα]). However, the mechanisms by which mitochondrial content in lower vertebrates such as fish is controlled are less studied. In my study I investigate underlying mechanisms of the phenomenon that many fish species alter mitochondrial enzyme activities, such as cytochrome c oxidase (COX) in response to low temperatures. In particular, I investigated (i) if the phenomenon of mitochondrial biogenesis during cold-acclimation is related to fish phylogeny, (ii) what role PGC-1α and other transcription factors play in mitochondrial biogenesis in fish, and (iii) if mRNA decay rates are important in the transcriptional control of a multimeric protein like COX. This study shows that mitochondrial biogenesis does not follow a phylogenetic pattern: while distantly related species displayed the same response to low temperatures, closely related species showed opposite responses. In species exhibiting mitochondrial biogenesis, little evidence was found for PGC-1α as a master regulator, whereas NRF-1 is supported to be an important regulator in mitochondrial biogenesis in fish. Further, there was little support for other transcription factors (NRF-2, ERRα, TRα-1, RXRα) to be part of the regulatory network. Lastly, results on the post-transcriptional control mechanism of mRNA decay indicate that this mechanism is important in the regulation of COX under mitochondrial biogenesis: it accounts for up to 30% of the change in subunit transcript levels. In summary, there is no simple temperature-dependent mitochondrial response ubiquitous in fish. Further, the pathways controlling mitochondrial content in fish differ from mammals in the important master regulator PGC-1α, however, NRF-1 is important in regulating cold-induced mitochondrial biogenesis in fish. Lastly, COX subunit mRNA decay rates seem to have a part in controlling COX amounts during mitochondrial biogenesis.

Subjects/Keywords: Cytochrome c Oxidase ; Transcription Factors ; PGC-1 ; Thermal Acclimation ; Fish ; Mitochondrial Biogenesis

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APA (6^th Edition):

Bremer, K. (2013). Environmental Sensitivity of Mitochondrial Gene Expression in Fish . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/8433

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Bremer, Katharina. “Environmental Sensitivity of Mitochondrial Gene Expression in Fish .” 2013. Thesis, Queens University. Accessed January 22, 2021. http://hdl.handle.net/1974/8433.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Bremer, Katharina. “Environmental Sensitivity of Mitochondrial Gene Expression in Fish .” 2013. Web. 22 Jan 2021.

Vancouver:

Bremer K. Environmental Sensitivity of Mitochondrial Gene Expression in Fish . [Internet] [Thesis]. Queens University; 2013. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1974/8433.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Bremer K. Environmental Sensitivity of Mitochondrial Gene Expression in Fish . [Thesis]. Queens University; 2013. Available from: http://hdl.handle.net/1974/8433

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Virginia Commonwealth University

11. Gomez-Arroyo, Jose. Metabolic Remodeling and Mitochondrial Dysfunction in Maladaptive Right Ventricular Hypertrophy Secondary to Pulmonary Arterial Hypertension.

Degree: PhD, Biochemistry, 2013, Virginia Commonwealth University

URL: https://doi.org/10.25772/6Z1D-NV83 ; https://scholarscompass.vcu.edu/etd/3257

► Right ventricular dysfunction is the most frequent cause of death in patients with pulmonary arterial hypertension. Although abnormal energy substrate use has been implicated in… (more)

▼ Right ventricular dysfunction is the most frequent cause of death in patients with pulmonary arterial hypertension. Although abnormal energy substrate use has been implicated in the development of chronic left heart failure, data describing such metabolic remodeling in failing right ventricular tissue remain incomplete. In the present dissertation we sought to characterize metabolic gene expression changes and mitochondrial dysfunction in functional and dysfunctional RV hypertrophy. Two different rat models of RV hypertrophy were studied. The model of right ventricular failure (SU5416/hypoxia) exhibited a significantly decreased gene expression of peroxisome proliferator-activated receptor- coactivator-1α, peroxisome proliferator- activated receptor-α and estrogen-related receptor-α. The expression of multiple peroxisome proliferator-activated receptor- coactivator-1α target genes required for fatty acid oxidation was similarly decreased. Decreased peroxisome proliferator-activated receptor- coactivator-1α expression was also associated with a net loss of mitochondrial protein and oxidative capacity. Reduced mitochondrial number was associated with a downregulation of transcription factor A, mitochondrial, and other genes required for mitochondrial biogenesis. Electron microscopy demonstrated that, in right ventricular failure tissue, mitochondria had abnormal shape and size. Lastly, respirometric analysis demonstrated that mitochondria isolated from right ventricular failure tissue had a significantly reduced ADP- stimulated (state 3) rate for complex I. Conversely, functional right ventricular hypertrophy in the pulmonary artery banding model showed normal expression of peroxisome proliferator-activated receptor- coactivator-1α, whereas the expression of fatty acid oxidation genes was either preserved or unregulated. Moreover, pulmonary artery banding-right ventricular tissue exhibited preserved transcription factor A mitochondrial expression and mitochondrial respiration despite elevated right ventricular pressure-overload. We conclude that right ventricular dysfunction, but not functional right ventricular hypertrophy in rats, demonstrates a gene expression profile compatible with a multilevel impairment of fatty acid metabolism and significant mitochondrial dysfunction, partially independent of chronic pressure-overload. Advisors/Committee Members: Norbert Voelkel.

Subjects/Keywords: PGC-1; mitochondria; right ventricle; right ventricular failure; Biochemistry, Biophysics, and Structural Biology; Life Sciences

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APA (6^th Edition):

Gomez-Arroyo, J. (2013). Metabolic Remodeling and Mitochondrial Dysfunction in Maladaptive Right Ventricular Hypertrophy Secondary to Pulmonary Arterial Hypertension. (Doctoral Dissertation). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/6Z1D-NV83 ; https://scholarscompass.vcu.edu/etd/3257

Chicago Manual of Style (16^th Edition):

Gomez-Arroyo, Jose. “Metabolic Remodeling and Mitochondrial Dysfunction in Maladaptive Right Ventricular Hypertrophy Secondary to Pulmonary Arterial Hypertension.” 2013. Doctoral Dissertation, Virginia Commonwealth University. Accessed January 22, 2021. https://doi.org/10.25772/6Z1D-NV83 ; https://scholarscompass.vcu.edu/etd/3257.

MLA Handbook (7^th Edition):

Gomez-Arroyo, Jose. “Metabolic Remodeling and Mitochondrial Dysfunction in Maladaptive Right Ventricular Hypertrophy Secondary to Pulmonary Arterial Hypertension.” 2013. Web. 22 Jan 2021.

Vancouver:

Gomez-Arroyo J. Metabolic Remodeling and Mitochondrial Dysfunction in Maladaptive Right Ventricular Hypertrophy Secondary to Pulmonary Arterial Hypertension. [Internet] [Doctoral dissertation]. Virginia Commonwealth University; 2013. [cited 2021 Jan 22]. Available from: https://doi.org/10.25772/6Z1D-NV83 ; https://scholarscompass.vcu.edu/etd/3257.

Council of Science Editors:

Gomez-Arroyo J. Metabolic Remodeling and Mitochondrial Dysfunction in Maladaptive Right Ventricular Hypertrophy Secondary to Pulmonary Arterial Hypertension. [Doctoral Dissertation]. Virginia Commonwealth University; 2013. Available from: https://doi.org/10.25772/6Z1D-NV83 ; https://scholarscompass.vcu.edu/etd/3257

Boston University

12. Charles, Quincy. Investigation of the pathological function of PGC1B in the retinal pigment epithelium and its implications for age-related macular degeneration.

Degree: MS, Medical Sciences, 2017, Boston University

URL: http://hdl.handle.net/2144/23750

► Age-Related Macular Degeneration (AMD) is a retinal eye disease that is the leading cause of blindness in those over 50 years of age throughout the… (more)

▼ Age-Related Macular Degeneration (AMD) is a retinal eye disease that is the leading cause of blindness in those over 50 years of age throughout the developed world. Oxidative and metabolic dysfunction of the retinal pigment epithelium (RPE) has been shown to play an important role in AMD. However, the mechanism of dysfunction in the RPE is poorly understood. The peroxisome proliferator-activated receptor-gamma coactivator 1α and β (PGC1A and PGC1B) are coactivators that interact with transcription factors to regulate mitochondria metabolism. In a previous study, it was demonstrated that one of the isoforms, PGC1A, protects RPE cells from oxidative stress through the upregulation of transcription factors that regulate important antioxidant enzymes. There is experimental and clinical evidence that demonstrates that PGC1B may play a deleterious role in the RPE cell. The objective of this study is to characterize the pathological effect of PGC1B on the RPE cell. PGC1B was overexpressed in the human retinal pigment epithelium cell line (ARPE-19) and expression of the PGC1 isoforms and their main gene targets was evaluated using quantitative polymerase chain reaction (qPCR). Cell death was evaluated under basal and pro-oxidant conditions by quantification of lactate dehydrogenase (LDH) release from the RPE cell. The effect of PGC1B gain of function on the RPE pro-angiogenic function was evaluated using the choroid explant sprouting assay and by testing the proliferative, migratory, and tube formation potential of RPE-derived conditioned media on the rhesus monkey chorioretinal cell line (RF/6A). Quantitative PCR analysis showed that overexpression of PGC1B in ARPE-19 cells leads to increased mitochondrial metabolism and decreased antioxidant enzyme expression, causing oxidative stress. After treatment with H2O2, PGC1B overexpression caused ARPE-19 cells to become more susceptible to cytotoxicity. The ex vivo choroid sprouting assay demonstrated that PGC1B overexpression in RPE is pro-angiogenic. However, cell proliferation as measured by MTT and the cell migration assay provided conflicting results on the pro-angiogenic effect of PGC1B. Previous research has demonstrated that oxidative stress in the RPE cell plays a role in AMD progression. It has been demonstrated in this study that PGC1B expression leads to increased mitochondrial metabolism and repression of antioxidant enzymes needed to prevent oxidative stress and dysfunction in the RPE cell. While experiments to test the effect of PGC1B on angiogenesis provided conflicting results, a different endothelial cell model may be better suited in demonstrating the pro-angiogenic effect of PGC1B. The hope is that the information provided from this study may be used to further our understanding of AMD and lead to the development of therapeutic targets to combat the effects of AMD.

Subjects/Keywords: Molecular biology; Angiogenesis; Metabolism; PGC-1; Age-related macular degeneration; Oxidative stress; Retinal pigemented epithelium

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APA (6^th Edition):

Charles, Q. (2017). Investigation of the pathological function of PGC1B in the retinal pigment epithelium and its implications for age-related macular degeneration. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/23750

Chicago Manual of Style (16^th Edition):

Charles, Quincy. “Investigation of the pathological function of PGC1B in the retinal pigment epithelium and its implications for age-related macular degeneration.” 2017. Masters Thesis, Boston University. Accessed January 22, 2021. http://hdl.handle.net/2144/23750.

MLA Handbook (7^th Edition):

Charles, Quincy. “Investigation of the pathological function of PGC1B in the retinal pigment epithelium and its implications for age-related macular degeneration.” 2017. Web. 22 Jan 2021.

Vancouver:

Charles Q. Investigation of the pathological function of PGC1B in the retinal pigment epithelium and its implications for age-related macular degeneration. [Internet] [Masters thesis]. Boston University; 2017. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/2144/23750.

Council of Science Editors:

Charles Q. Investigation of the pathological function of PGC1B in the retinal pigment epithelium and its implications for age-related macular degeneration. [Masters Thesis]. Boston University; 2017. Available from: http://hdl.handle.net/2144/23750

University of Cambridge

13. Valli, Haseeb. Atrial arrhythmogenesis in a murine model of mitochondrial insufficiency.

Degree: PhD, 2019, University of Cambridge

URL: https://doi.org/10.17863/CAM.41673 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782943

► Age-related atrial arrhythmias including atrial fibrillation are frequently encountered in clinical practice and are associated with significant mortality and morbidity. A putative role for chronic… (more)

▼ Age-related atrial arrhythmias including atrial fibrillation are frequently encountered in clinical practice and are associated with significant mortality and morbidity. A putative role for chronic mitochondrial impairment in their pathogenesis was investigated using a murine model with homozygous deficiency of the transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator-1 β (Pgc-1β-/-). Pgc-1β regulates mitochondrial biogenesis and function, and unlike other murine models of mitochondrial dysfunction Pgc-1β-/- mice have a mild cardiac phenotype, devoid of confounding contractile dysfunction. All experiments were performed in young (12-16 weeks) and aged (>52 weeks) Pgc-1β-/- mice and compared to aged-matched wild type (WT) controls. Sharp microelectrode recordings of cellular action potentials (AP) in a whole-heart Langendorff-perfused system revealed that the Pgc-1β-/- genotype was associated with an atrial arrhythmic phenotype that progressed with age. Young and aged Pgc-1β-/- hearts showed evidence of slowed AP conduction at the cellular level, through deficits in maximum rates of AP depolarization (dV/dt)max, and at the tissue level through prolonged AP latencies. Action potential duration (APD) was also significantly shorter in Pgc-1β-/- hearts at high heart rates. APD restitution has been linked to the pathogenesis of ventricular fibrillation and more recently AF. However in the present work the incidence of alternans or steepness of the restitution curves did not correlate with arrhythmic tendency. Loose patch clamp measurements demonstrated that Pgc-1β−/− atria had significantly lower inward Na+ currents than that of WT preparations, correlating to the differences in (dV/dt)max values. No differences in delayed outward (K+) currents were evident. Morphometric analysis revealed that Pgc-1β deficiency was associated with accelerated fibrosis, with aged Pgc-1β-/- hearts displaying the greatest fibrotic change. The Pgc-1β-/- murine model of chronic mitochondrial impairment results in an age-related atrial arrhythmic phenotype through adverse electrical and structural remodelling producing an atrial substrate promoting AP reentry and arrhythmia persistence.

Subjects/Keywords: Atrial fibrillation; arrhythmia; mitochondrial; metabolic; peroxisome proliferator-activated receptor ? coactivator-1 ß; Pgc-1ß

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APA (6^th Edition):

Valli, H. (2019). Atrial arrhythmogenesis in a murine model of mitochondrial insufficiency. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.41673 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782943

Chicago Manual of Style (16^th Edition):

Valli, Haseeb. “Atrial arrhythmogenesis in a murine model of mitochondrial insufficiency.” 2019. Doctoral Dissertation, University of Cambridge. Accessed January 22, 2021. https://doi.org/10.17863/CAM.41673 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782943.

MLA Handbook (7^th Edition):

Valli, Haseeb. “Atrial arrhythmogenesis in a murine model of mitochondrial insufficiency.” 2019. Web. 22 Jan 2021.

Vancouver:

Valli H. Atrial arrhythmogenesis in a murine model of mitochondrial insufficiency. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Jan 22]. Available from: https://doi.org/10.17863/CAM.41673 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782943.

Council of Science Editors:

Valli H. Atrial arrhythmogenesis in a murine model of mitochondrial insufficiency. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://doi.org/10.17863/CAM.41673 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782943

University of Gothenburg / Göteborgs Universitet

14. Hammarstedt, Ann 1975-. Molecular characterization of insulin resistance in the adipose tissue and the effects of thiazolidinediones.

Degree: 2005, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/16478

► Type 2 diabetes is the most common metabolic disorder today and has reached epidemic proportions in many contries. Insulin resistance plays a central role in… (more)

▼ Type 2 diabetes is the most common metabolic disorder today and has reached epidemic proportions in many contries. Insulin resistance plays a central role in the pathogenesis of Type 2 diabetes and can be present for a decade or more before onset of the disease. During this time, many of the abnormalities and complications associated with Type 2 diabetes are initiated. Studies in, and identification of, pre-diabetic individuals are therefore important for the prevention and understanding of the cause of Type 2 diabetes. Thiazolidinediones (TZD) is a group of agents used in the treatment of Type 2 diabetes. However, our knowledge about their mode of action is still incomplete.The aims of this thesis were: 1) To study the effect of TZD treatment on key insulin signaling molecules in cultured skeletal muscle cells (Paper I); 2) To examine the expression of PGC-alpha in adipose tissue of non-diabetic but insulin-resistant individuals as well as its relation to insulin sensitivity and different markers involved in insulin action (Paper II); 3) To characterize the IRS-1 expression in the adipose tissue and its potential role as a marker for insulin resistance and early atherosclerosis (Paper III); 4) To examine if short-term treatment with TZD improves insulin sensitivity in non-diabetic but insulin-resistant individuals, and if this is associated with an improvement in the dysregulated adipose tissue that we have documented to be associated with insulin resistance (Paper IV). In Paper I, L6 skeletal muscles were used to study the effects of TZD on gene and protein expression of major insulin signaling molecules. TZD treatment increased the expression of IRS-1, possibly through an indirect mechanism. In Paper II, we show that PGC-alpha is expressed in human isolated adipocytes and that its expression is decreased in individuals characterized by low protein expression of IRS-1 in the adipose cells and reduced insulin sensitivity. In Paper III, we report that a low IRS-1 protein expression in the adipose cells seems to be a more sensitive marker for identifying individuals at risk of developing Type 2 diabetes and atherosclerosis, compared to a known genetic predisposition for the disease. Furthermore, the individuals expressing low IRS-1 protein in the adipose cells display lower circulating levels of adiponectin and show attenuated expression of several genes related to adipogenesis in the adipose tissue. In Paper IV, we show that short-term treatment with TZD increases the insulin sensitivity and that this is associated with an improvement in some, but not all, markers of a dysregulated adipose tissue.In conclusion, low IRS-1 protein expression in the adipose cells is a marker for identifying individuals with reduced insulin sensitivity. These individuals are also characterized by a reduced expression of PGC-alpha, attenuated adipocyte differentiation and low levels of circulating adiponectin. TZD increases the expression of IRS-1 in vitro in cultured skeletal muscle cells. In vivo, however, short-term treatment (3 wks)…

Subjects/Keywords: IRS-1; PGC-1; adiponectin; insulin resistance; TZD

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APA (6^th Edition):

Hammarstedt, A. 1. (2005). Molecular characterization of insulin resistance in the adipose tissue and the effects of thiazolidinediones. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/16478

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hammarstedt, Ann 1975-. “Molecular characterization of insulin resistance in the adipose tissue and the effects of thiazolidinediones.” 2005. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed January 22, 2021. http://hdl.handle.net/2077/16478.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hammarstedt, Ann 1975-. “Molecular characterization of insulin resistance in the adipose tissue and the effects of thiazolidinediones.” 2005. Web. 22 Jan 2021.

Vancouver:

Hammarstedt A1. Molecular characterization of insulin resistance in the adipose tissue and the effects of thiazolidinediones. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2005. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/2077/16478.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hammarstedt A1. Molecular characterization of insulin resistance in the adipose tissue and the effects of thiazolidinediones. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2005. Available from: http://hdl.handle.net/2077/16478

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Université Montpellier II

15. Abdel Khalek, Waed. Sirt3, une déacetylase mitochondriale NAD+dépendante, est impliquée dans la regulation de la différenciation des myoblastes : SIRT3, a mitochondrial NAD+-dependent deacetylase is involved in the regulation of myoblast differentiation.

Degree: Docteur es, Biologie Santé, 2013, Université Montpellier II

URL: http://www.theses.fr/2013MON20022

► Sirt3, une des sept sirtuines chez les mammifères, est une déacétylase mitochondriale NAD+-dépendante qui joue un rôle dans le contrôle des facteurs clés de plusieurs… (more)

▼ Sirt3, une des sept sirtuines chez les mammifères, est une déacétylase mitochondriale NAD+-dépendante qui joue un rôle dans le contrôle des facteurs clés de plusieurs voies métaboliques. Sirt3 déacétyle et active un grand nombre d'enzymes mitochondriales impliquées dans l'activité de la chaîne respiratoire, la production d'ATP, le cycle de Krebs, ainsi que le cycle de l'urée. Parallèlement à son rôle dans le métabolisme énergétique, l'activité mitochondriale intervient également dans l'induction de l'apoptose ainsi que dans la régulation de la prolifération et la différenciation cellulaires. En particulier les travaux du laboratoire ont montré qu'il existe une véritable régulation de la différenciation myogénique par l'activité mitochondriale. Comme Sirt3 régule l'activité mitochondriale, nous nous sommes intéressés à étudier l'implication de cette sirtuine dans la différenciation des myoblastes. Dans une première partie, nous avons évalué l'expression endogène de Sirt3 au cours de la différenciation des myoblastes murins C2C12, puis étudié l'effet de son inhibition sur le processus de différenciation et sur l'activité mitochondriale. Nous avons montré que l'expression de Sirt3 endogène augmente après induction de la différenciation des C2C12. Une inhibition stable de l'expression de Sirt3 par interférence (Short hairpin Sirt3, shSirt3) entraîne : 1) un blocage de la différenciation terminale des C2C12 reflété par une chute significative de l'index de fusion ainsi que de l'expression des marqueurs myogéniques MyoD, Myogénine et troponine T ; 2) une diminution de l'activité mitochondriale reflétée par une altération de l'expression de PGC-1alpha, VDAC et citrate synthase, et une diminution des activités enzymatiques des complexes de la chaîne respiratoire et de la respiration maximale des myoblastes ; 3) une augmentation de la production de DROs. Ces résultats suggèrent un rôle important de Sirt3 dans la différenciation des myoblastes, en relation avec son influence sur l'activité mitochondriale.Dans une seconde partie, nous avons évalué l'importance de Sirt3 in vivo sur le développement et le métabolisme du tissu musculaire en étudiant le phénotype de souris surexprimant l'isoforme courte (MCK-SIRT3M3) ou l'isoforme longue (MCK-SIRT3M1) de Sirt3 spécifiquement dans le muscle squelettique. Nos premiers résultats obtenus à l'âge de 3 mois montrent que la capacité oxydative des souris MCK-SIRT3M1 est plus faible et celle des souris MCK-SIRT3M3 plus élevée par rapport aux souris sauvages. Les souris MCK-SIRT3M3 présentent une atrophie musculaire dès l'âge de trois mois alors que la capacité musculaire et l'activité mitochondriale dans les muscles de ces souris ne sont pas modifiées. Avec l'âge, le phénotype des souris surexprimant l'isoforme M3 dans le muscle est plus marqué : l'atrophie s'accentue, le nombre de mitochondries augmente, et l'expression de la myosine de type 1 augmente alors que l'expression des myosines de type II diminue. Ces données indiquent que l'isoforme courte de Sirt 3 aurait une influence dans le… Advisors/Committee Members: Cabello, Chantal (thesis director), Chabi, Béatrice (thesis director).

Subjects/Keywords: Muscle; Differenciation; Sirtuine 3; PGC-1α; Peroxisome proliferator-activated receptor gamma coactivator 1-alpha; Dérivés réactifs d'oxygeneSirtuine 1; Muscle; Differentiation; Sirtuin 3; PGC-1α; Peroxisome proliferator-activated receptor gamma coactivator 1-alpha; Reactive Oxygen species ROS; Sirtuin 1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Abdel Khalek, W. (2013). Sirt3, une déacetylase mitochondriale NAD+dépendante, est impliquée dans la regulation de la différenciation des myoblastes : SIRT3, a mitochondrial NAD+-dependent deacetylase is involved in the regulation of myoblast differentiation. (Doctoral Dissertation). Université Montpellier II. Retrieved from http://www.theses.fr/2013MON20022

Chicago Manual of Style (16^th Edition):

Abdel Khalek, Waed. “Sirt3, une déacetylase mitochondriale NAD+dépendante, est impliquée dans la regulation de la différenciation des myoblastes : SIRT3, a mitochondrial NAD+-dependent deacetylase is involved in the regulation of myoblast differentiation.” 2013. Doctoral Dissertation, Université Montpellier II. Accessed January 22, 2021. http://www.theses.fr/2013MON20022.

MLA Handbook (7^th Edition):

Abdel Khalek, Waed. “Sirt3, une déacetylase mitochondriale NAD+dépendante, est impliquée dans la regulation de la différenciation des myoblastes : SIRT3, a mitochondrial NAD+-dependent deacetylase is involved in the regulation of myoblast differentiation.” 2013. Web. 22 Jan 2021.

Vancouver:

Abdel Khalek W. Sirt3, une déacetylase mitochondriale NAD+dépendante, est impliquée dans la regulation de la différenciation des myoblastes : SIRT3, a mitochondrial NAD+-dependent deacetylase is involved in the regulation of myoblast differentiation. [Internet] [Doctoral dissertation]. Université Montpellier II; 2013. [cited 2021 Jan 22]. Available from: http://www.theses.fr/2013MON20022.

Council of Science Editors:

Abdel Khalek W. Sirt3, une déacetylase mitochondriale NAD+dépendante, est impliquée dans la regulation de la différenciation des myoblastes : SIRT3, a mitochondrial NAD+-dependent deacetylase is involved in the regulation of myoblast differentiation. [Doctoral Dissertation]. Université Montpellier II; 2013. Available from: http://www.theses.fr/2013MON20022

University of Ottawa

16. Burt, Matthew. Resveratrol as a Novel Therapeutic Agent for Treating Duchenne Muscular Dystrophy .

Degree: 2013, University of Ottawa

URL: http://hdl.handle.net/10393/26273

► Duchenne Muscular Dystrophy (DMD) is an x-linked neuromuscular disease that is caused by an absence of dystrophin protein, rendering skeletal muscle more susceptible to contraction-induced… (more)

Subjects/Keywords: resveratrol; skeletal muscle; utrophin; dystrophin; mdx; duchenne muscular dystropy; slow oxidative myogenic program; sirt1; pgc-1 alpha

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Burt, M. (2013). Resveratrol as a Novel Therapeutic Agent for Treating Duchenne Muscular Dystrophy . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/26273

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Burt, Matthew. “Resveratrol as a Novel Therapeutic Agent for Treating Duchenne Muscular Dystrophy .” 2013. Thesis, University of Ottawa. Accessed January 22, 2021. http://hdl.handle.net/10393/26273.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Burt, Matthew. “Resveratrol as a Novel Therapeutic Agent for Treating Duchenne Muscular Dystrophy .” 2013. Web. 22 Jan 2021.

Vancouver:

Burt M. Resveratrol as a Novel Therapeutic Agent for Treating Duchenne Muscular Dystrophy . [Internet] [Thesis]. University of Ottawa; 2013. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10393/26273.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Burt M. Resveratrol as a Novel Therapeutic Agent for Treating Duchenne Muscular Dystrophy . [Thesis]. University of Ottawa; 2013. Available from: http://hdl.handle.net/10393/26273

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Tennessee – Knoxville

17. Kearns, Jamie Ann. Beneficial effects of naringenin and indomethacin on white and brown adipocytes.

Degree: MS, Nutrition, 2016, University of Tennessee – Knoxville

URL: https://trace.tennessee.edu/utk_gradthes/4265

► As obesity continues to grow and medical costs in the United States are estimated at $147 billion annually, novel ways to prevent and treat… (more)

▼ As obesity continues to grow and medical costs in the United States are estimated at $147 billion annually, novel ways to prevent and treat obesity are needed. One approach is to promote thermogenesis to improve energy balance by increasing the activities of thermogenic brown and beige adipocytes. Naringenin, a citrus flavanone, has been shown to act as anti-inflammatory and lipid lowering agent as well as activate PPARgamma. However, it is unclear whether it can activate thermogenic activity in white adipocytes, i.e., promote formation of beige adipocytes. Indomethacin (INDO) is an FDA approved drug used to treat pain related to inflammation by inhibiting cyclooxygenase (COX). It has been demonstrated that INDO is a PPARgamma agonist and is protective against weight gain in mice fed a high fat and high sucrose diet. Whether INDO independently induces brown adipocyte differentiation has not been studied. In this thesis, I investigated the effect of naringenin combined with isoproterenol, a beta- adrenergic receptor agonist on thermogenic activation of a common white adipocyte cell line, 3T3-L1. In addition, I investigated whether INDO induces brown adipocyte differentiation. 3T3- L1 cells were differentiated into mature adipocytes with a standard differentiation cocktail in the presence of naringenin and then stimulated with isoproterenol. While naringenin had little effect at the basal level, it significantly increased mRNA and protein expression of UCP-1 and PGC- 1alpha, browning marker genes. Moreover, naringenin increased mitochondrial DNA, which is indicative of increased mitochondrial biogenesis. The results suggest that in addition to increased UCP-1 expression, naringenin can promote up regulation of PGC-1alpha, leading to increased mitochondrial biogenesis in thermogenic activation of 3T3-L1. To study the effects of INDO on brown adipocyte differentiation I differentiated brown preadipocytes in the presence of increasing doses of INDO using a modified differentiation protocol. INDO dose-dependently increased lipid accumulation and mRNA expression of brown specific marker genes PGC-1alpha, UCP-1 and PRDM16. Protein expression of PGC-1alpha and UCP-1 was confirmed by western analysis. Consistently, INDO dose-dependently increased mitochondrial biogenesis. Mechanistically, INDO increased PPAR responsive promoter activities. These results suggest that INDO may promote brown adipogenesis through activation of PPARgamma. Advisors/Committee Members: Ling Zhao, Guoxun Chen, Ahmed Bettaieb.

Subjects/Keywords: UCP-1; PGC-1alpha; indomethacin; naringenin; brown adipocyte; mitochondrial biogenesis; Molecular, Genetic, and Biochemical Nutrition; Nutrition

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kearns, J. A. (2016). Beneficial effects of naringenin and indomethacin on white and brown adipocytes. (Thesis). University of Tennessee – Knoxville. Retrieved from https://trace.tennessee.edu/utk_gradthes/4265

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Kearns, Jamie Ann. “Beneficial effects of naringenin and indomethacin on white and brown adipocytes.” 2016. Thesis, University of Tennessee – Knoxville. Accessed January 22, 2021. https://trace.tennessee.edu/utk_gradthes/4265.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Kearns, Jamie Ann. “Beneficial effects of naringenin and indomethacin on white and brown adipocytes.” 2016. Web. 22 Jan 2021.

Vancouver:

Kearns JA. Beneficial effects of naringenin and indomethacin on white and brown adipocytes. [Internet] [Thesis]. University of Tennessee – Knoxville; 2016. [cited 2021 Jan 22]. Available from: https://trace.tennessee.edu/utk_gradthes/4265.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kearns JA. Beneficial effects of naringenin and indomethacin on white and brown adipocytes. [Thesis]. University of Tennessee – Knoxville; 2016. Available from: https://trace.tennessee.edu/utk_gradthes/4265

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

18. Matiello, Renata. Expressão do Coativador-1 do Peroxisome Proliferator-Activated Receptor- (PGC-1) em fígado e músculos esqueléticos soleus e plantaris de ratos machos Wistar submetidos ao exercício físico voluntário crônico.

Degree: Mestrado, Endocrinologia, 2009, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5135/tde-10092009-143555/ ;

► INTRODUÇÃO: A Peroxisome Proliferator Activated Receptor- - Coactivator 1 ( PGC-1 e ) é proteína responsável pela conexão entre estímulos ambientais e resposta metabólica celular.… (more)

▼ INTRODUÇÃO: A Peroxisome Proliferator Activated Receptor- - Coactivator 1 ( PGC-1 e ) é proteína responsável pela conexão entre estímulos ambientais e resposta metabólica celular. Sua presença é importante em tecidos adiposo, hepático e muscular esquelético e, em animais, em tecido adiposo marrom. Interage com receptores nucleares modulando a biogênese mitocondrial e mantendo o equilíbrio termo energético celular com o meio ambiente. A redução da expressão de PGC-1 e da oxidação fosforilativa tem sido associada à resistência à insulina em doenças como Diabetes Mellitus tipo 2 e Síndrome Metabólica. OBJETIVOS: Avaliar o efeito do exercício na expressão da PGC-1 em tecidos alvos da insulina, como o fígado e músculos esquléticos soleus ( SOL ) e plantaris ( PLA ) de ratos machos Wistar e correlacioná-lo com a sensibilidade à insulina. METODOLOGIA: Ratos machos Wistar 190±15 g, n = 24, randomizados em 2 grupos: Ex ( exercício físico ) e Sd ( sedentário ) colocados respectivamente, em roda de atividade ou gaiolas comuns durante cinco semanas. Ao final do período, após jejum de quatro horas, foi colhido sangue para dosagens de glicose ( GLI ), insulina ( INS ) e ácidos graxos livres ( AGL ) e, em seguida, foram submetidos ao Teste de Supressão da Glicose e Insulina Endógenas com infusão durante 180 minutos de solução GLI ( 20mg/kg/min ) + INS ( 5 mU/kg/min ); amostras de sangue foram colhidas aos 140, 150, 160, 170 e 180 minutos. Terminado o teste e ainda sob anestesia, foram retirados os tecidos: fígado ( FG ) e músculos esquléticos ( PLA e SOL ), os quais foram imediatamente congelados e mantidos a -70ºC para posteriores análises. A expressão da PGC-1 foi avaliada pelo Western Blot com anticorpo policlonal anti- PGC-1. Análise estatística por teste t Student não-pareado e nível de significância 5%. RESULTADOS: Os dados se referem à média e erro padrão médio dos valores individuais das amostras. A distância percorrida na última semana ( km/dia ) pelo grupo Ex foi eficaz ( 5,61 ± 0,67 ). Não houve diferença no peso ( g ) dos ratos entre os grupos Ex e Sd ( 355,85 ± 9,51 x 375,68 ± 5,30 ) NS. Os valores de GLI jejum ( mg/dl ) foram semelhantes entre os grupos ( 117,6 ± 3,7 x 122,4 ± 2,6 ) NS. Entretanto, INS e AGL foram menores no grupo Ex: INS ( ng/ml ) ( 0,68 ± 0,12 x 1,45 ± 0,14 ) p < 0,001 e AGL ( mEq/L ) ( 1,12 ± 0,11 x 1,60 ± 0,11 ) p < 0,006. Durante o teste de supressão, os valores de GLI e INS na fase de estabilidade foram semelhantes entre grupos ( expressos em área sob a curva ): AUC GLI ( mg/dl/min ) ( 2,77 ± 0,12 x 2,95 ± 0,07 ) NS; AUC INS ( ng/ml/min ) ( 0,81 ± 0,15 x 0,99 ± 0,09 ) NS. A expressão da PGC-1 foi maior no PLA de ratos do grupo Ex e, em FG e SOL foi semelhante entre os grupos. CONCLUSÃO: O exercício físico durante 5 semanas em roda de atividade voluntária, aumentou a sensibilidade à insulina e a oxidação de ácidos graxos livres no jejum. A melhora da sensibilidade à insulina esteve associada à maior expressão da PGC-1 somente em músculo PLA. Estes dados sugerem que o aumento da sensibilidade à… Advisors/Committee Members: Santos, Rosa Ferreira dos.

Subjects/Keywords: Exercício físico; Insulin resistance; Músculo esquelético plantaris; Músculo esqulético soleus; PGC-1; PGC-1; Physical exercise; Resistência à insulina; Roda de atividade; Skeletal plantaris muscle; Skeletal soleus muscle; Voluntary wheel running

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Matiello, R. (2009). Expressão do Coativador-1 do Peroxisome Proliferator-Activated Receptor- (PGC-1) em fígado e músculos esqueléticos soleus e plantaris de ratos machos Wistar submetidos ao exercício físico voluntário crônico. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5135/tde-10092009-143555/ ;

Chicago Manual of Style (16^th Edition):

Matiello, Renata. “Expressão do Coativador-1 do Peroxisome Proliferator-Activated Receptor- (PGC-1) em fígado e músculos esqueléticos soleus e plantaris de ratos machos Wistar submetidos ao exercício físico voluntário crônico.” 2009. Masters Thesis, University of São Paulo. Accessed January 22, 2021. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-10092009-143555/ ;.

MLA Handbook (7^th Edition):

Matiello, Renata. “Expressão do Coativador-1 do Peroxisome Proliferator-Activated Receptor- (PGC-1) em fígado e músculos esqueléticos soleus e plantaris de ratos machos Wistar submetidos ao exercício físico voluntário crônico.” 2009. Web. 22 Jan 2021.

Vancouver:

Matiello R. Expressão do Coativador-1 do Peroxisome Proliferator-Activated Receptor- (PGC-1) em fígado e músculos esqueléticos soleus e plantaris de ratos machos Wistar submetidos ao exercício físico voluntário crônico. [Internet] [Masters thesis]. University of São Paulo; 2009. [cited 2021 Jan 22]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5135/tde-10092009-143555/ ;.

Council of Science Editors:

Matiello R. Expressão do Coativador-1 do Peroxisome Proliferator-Activated Receptor- (PGC-1) em fígado e músculos esqueléticos soleus e plantaris de ratos machos Wistar submetidos ao exercício físico voluntário crônico. [Masters Thesis]. University of São Paulo; 2009. Available from: http://www.teses.usp.br/teses/disponiveis/5/5135/tde-10092009-143555/ ;

University of New Mexico

19. Vaughan, Roger. Effects of dietary stimulators of metabolism and mitochondrial biogenesis in vitro and in vivo: Implications for metabolic disease.

Degree: Health, Exercise, and Sports Sciences, 2014, University of New Mexico

URL: http://hdl.handle.net/1928/24352

► Background: Commercially available dietary products advertised to promote weight loss are an under researched but heavily purchased commodity in the United States. Despite only limited… (more)

▼ Background: Commercially available dietary products advertised to promote weight loss are an under researched but heavily purchased commodity in the United States. Despite only limited evidence, interest in dietary supplements continues to increase. Obesity is an increasingly prevalent and preventable morbidity with multiple behavioral, surgical and pharmacological interventions currently available. Commercially available dietary supplements are often advertised to stimulate metabolism and cause rapid weight and/or fat loss, although few well controlled studies have demonstrated such effects. This work uniquely summarizes the current evidence evaluating the efficacy of several over-the-counter thermogenic products for their effects on resting energy expenditure. Additionally, this work outlines the important therapeutic benefits provided by dietary stimulators of metabolism and peroxisome proliferator-activated receptor gamma co-activator 1 (PGC-1) in skeletal muscle. Our work uniquely describes the effects of a commercially available dietary supplement on resting metabolic rate in humans as well as the metabolic and biochemical effects in vitro. Methods: Human rhabdomyosarcoma cells (RD) and mouse myoblasts (C2C12) were cultured under standard conditions and treated with various doses of a commercially available supplement (RF) for various durations and assessed for changes in metabolism, metabolic gene expression and mitochondrial content. Additionally, human subjects ingested either placebo or RF in a double-blind placebo controlled fashion and metabolic rate and blood pressure were measured at 3 time points for 3 hours post-ingestion. Results: RF enhanced metabolism, metabolic gene expression, and mitochondrial content in both cell models. RF also enhanced energy expenditure in human male subjects without altering substrate utilization. RF also significantly increased systolic blood pressure. Conclusion: RF appears to increase metabolism immediately following ingestion, although additional research is needed to assess safety and efficacy for human weight loss. Advisors/Committee Members: Mermier, Christine, Conn, Carole, Kravitz, Len, Bisoffi, Marco, Trujillo, Kristina.

Subjects/Keywords: Thermogenic Supplements; Fat Burners; Metabolic Rate; Obesity; Caffeine; Phytochemicals; 5' adenosine monophosphate-activated protein kinase (AMPK); Peroxisome proliferator-activated receptor gamma co-activator 1 (PGC-1); Mitochondrial Biogenesis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Vaughan, R. (2014). Effects of dietary stimulators of metabolism and mitochondrial biogenesis in vitro and in vivo: Implications for metabolic disease. (Doctoral Dissertation). University of New Mexico. Retrieved from http://hdl.handle.net/1928/24352

Chicago Manual of Style (16^th Edition):

Vaughan, Roger. “Effects of dietary stimulators of metabolism and mitochondrial biogenesis in vitro and in vivo: Implications for metabolic disease.” 2014. Doctoral Dissertation, University of New Mexico. Accessed January 22, 2021. http://hdl.handle.net/1928/24352.

MLA Handbook (7^th Edition):

Vaughan, Roger. “Effects of dietary stimulators of metabolism and mitochondrial biogenesis in vitro and in vivo: Implications for metabolic disease.” 2014. Web. 22 Jan 2021.

Vancouver:

Vaughan R. Effects of dietary stimulators of metabolism and mitochondrial biogenesis in vitro and in vivo: Implications for metabolic disease. [Internet] [Doctoral dissertation]. University of New Mexico; 2014. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1928/24352.

Council of Science Editors:

Vaughan R. Effects of dietary stimulators of metabolism and mitochondrial biogenesis in vitro and in vivo: Implications for metabolic disease. [Doctoral Dissertation]. University of New Mexico; 2014. Available from: http://hdl.handle.net/1928/24352

Queens University

20. Scribbans, Trisha Dawn. The adaptive response of humans to exercise: Impact of exercise intensity, fibre-type specific responses and molecular patterns of response .

Degree: Kinesiology and Health Studies, 2016, Queens University

URL: http://hdl.handle.net/1974/14613

► In an attempt to improve the current understanding of the adaptive response to exercise in humans, this dissertation performed a series of studies designed to… (more)

▼ In an attempt to improve the current understanding of the adaptive response to exercise in humans, this dissertation performed a series of studies designed to examine the impact of training intensity and mode on aerobic capacity and performance, fibre-type specific adaptations to training, and individual patterns of response across molecular, morphological and genetic factors. Project1 determined that training intensity, session dose, baseline VO2max and total training volume do not influence the magnitude of change in VO2max by performing a meta-regression, and meta-analysis of 28 different studies. The intensity of training had no effect on the magnitude of increase in maximal oxygen uptake in young healthy participants, but similar adaptations were achieved with lower training doses following high intensity training. Project # 2 determined the acute molecular response, and training-induced adaptations in aerobic performance, aerobic capacity and muscle phenotype following high-intensity interval training (HIT) or endurance exercise (END). The acute molecular response (fibre recruitment and signal activation) and training-induced adaptations in aerobic capacity, aerobic performance, and muscle phenotype were similar following HIT and END. Project # 3 examined the impact of baseline muscle morphology and molecular characteristics on the training response, and if muscle adaptations are coordinated. The muscle phenotype of individuals who experience the largest improvements (high responders) were lower before training for some muscle characteristics and molecular adaptations were coordinated within individual participants. Project # 4 examined the impact of 2 different intensities of HIT on the expression of nuclear and mitochondrial encoded genes targeted by PGC-1α. A systematic upregulation of nuclear and mitochondrial encoded genes was not present in the early recovery period following acute HIT, but the expression of mitochondrial genes were coordinated at an individual level. Collectively, results from the current dissertation contribute to our understanding of the molecular mechanisms influencing skeletal muscle and whole-body adaptive responses to acute exercise and training in humans.

Subjects/Keywords: Fibre-specific responses ; Individual responses ; high-intensity interval training ; endurance exercise ; maximal aerobic capacity ; mitochondrial biogenesis ; endurance exercise ; skeletal muscle ; PGC-1 alpha ; exercise intensity

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APA (6^th Edition):

Scribbans, T. D. (2016). The adaptive response of humans to exercise: Impact of exercise intensity, fibre-type specific responses and molecular patterns of response . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/14613

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Scribbans, Trisha Dawn. “The adaptive response of humans to exercise: Impact of exercise intensity, fibre-type specific responses and molecular patterns of response .” 2016. Thesis, Queens University. Accessed January 22, 2021. http://hdl.handle.net/1974/14613.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Scribbans, Trisha Dawn. “The adaptive response of humans to exercise: Impact of exercise intensity, fibre-type specific responses and molecular patterns of response .” 2016. Web. 22 Jan 2021.

Vancouver:

Scribbans TD. The adaptive response of humans to exercise: Impact of exercise intensity, fibre-type specific responses and molecular patterns of response . [Internet] [Thesis]. Queens University; 2016. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1974/14613.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Scribbans TD. The adaptive response of humans to exercise: Impact of exercise intensity, fibre-type specific responses and molecular patterns of response . [Thesis]. Queens University; 2016. Available from: http://hdl.handle.net/1974/14613

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

York University

21. Wu, Michelle Victoria. Regulation of Thermogenic Capacity in White and Brown Adipose Tissues by Chronic Endurance Exercise and High-Fat Diet.

Degree: MSc -MS, Kinesiology & Health Science, 2015, York University

URL: http://hdl.handle.net/10315/30720

► This study investigated the effects of high-fat (HF) diet and chronic endurance exercise (Ex) on the regulation of thermogenic capacity in both brown adipose tissue… (more)

Subjects/Keywords: Kinesiology; Physiology; Biology; brown adipose tissue; adipose tissue; metabolism; fat; pgc-1a; ATGL; lipolysis; thermogenesis; UCP-1; p-AMPK; white adipose tissue; beige fat; thermogenic capacity; plasticity; uncoupling; FNDC5; irisin; muscle; palmitate oxidation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wu, M. V. (2015). Regulation of Thermogenic Capacity in White and Brown Adipose Tissues by Chronic Endurance Exercise and High-Fat Diet. (Masters Thesis). York University. Retrieved from http://hdl.handle.net/10315/30720

Chicago Manual of Style (16^th Edition):

Wu, Michelle Victoria. “Regulation of Thermogenic Capacity in White and Brown Adipose Tissues by Chronic Endurance Exercise and High-Fat Diet.” 2015. Masters Thesis, York University. Accessed January 22, 2021. http://hdl.handle.net/10315/30720.

MLA Handbook (7^th Edition):

Wu, Michelle Victoria. “Regulation of Thermogenic Capacity in White and Brown Adipose Tissues by Chronic Endurance Exercise and High-Fat Diet.” 2015. Web. 22 Jan 2021.

Vancouver:

Wu MV. Regulation of Thermogenic Capacity in White and Brown Adipose Tissues by Chronic Endurance Exercise and High-Fat Diet. [Internet] [Masters thesis]. York University; 2015. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10315/30720.

Council of Science Editors:

Wu MV. Regulation of Thermogenic Capacity in White and Brown Adipose Tissues by Chronic Endurance Exercise and High-Fat Diet. [Masters Thesis]. York University; 2015. Available from: http://hdl.handle.net/10315/30720

University of Gothenburg / Göteborgs Universitet

22. Ljungberg, Anna 1977-. The role of PPARalpha and growth hormone in hepatic lipid metaboism and atherosclerosis.

Degree: 2006, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/16865

► Dyslipidemia mainly results from oversecretion of apoB-containing lipoproteins from theliver and is one of the most important risk factors for the development of atherosclerosis.Growth hormone… (more)

▼ Dyslipidemia mainly results from oversecretion of apoB-containing lipoproteins from theliver and is one of the most important risk factors for the development of atherosclerosis.Growth hormone (GH) plays a key role in the regulation of lipoprotein metabolism and thus,disturbances in GH secretion are associated with dyslipidemia and cardiovascular disease.GH influences the activity of the nuclear hormone receptor peroxisome proliferator-activatedreceptor (PPAR)alpha, which regulates genes involved in lipid metabolism through interactionwith coactivators. PPARgamma coactivator-1 (PGC-1) has been shown to coactivate severaltranscription factors, including PPARalpha.GH transgenic mice on apoE-deficient background had larger atherosclerotic lesion area inthe thoracic aorta and more advanced lesions in aortic sinus compared to littermate controls.Changes in serum lipoproteins were most likely not involved in the accelerated lesionformation in GH transgenic mice since their lipoprotein profile was not worsened. Instead,higher blood pressure and an increased inflammatory response could contribute to thiseffect. Treatment of mice with a high dose of GH increased triglyceride secretion, serumapoB and cholesterol levels, whereas liver triglycerides were reduced. Most of the studiedeffects of GH were similar in PPARalpha-deficient and wild-type mice and thus independent ofPPARalpha. However, hepatic PPARgamma2 and Cyp4a10 mRNA expression were PPARalpha dependent,indicating that PPARalpha is important for the effect of GH on hepatic PPARgamma signaling and omega-oxidation. Treatment of mice and incubation of mouse hepatocytes with the PPARalpha agonistWy14,643 (Wy) resulted in hepatic triglyceride accumulation in parallel with increasedexpression of adipose differentiation-related protein (ADRP). Studies in mouse hepatocytesshowed that the increased triglyceride content was associated with inhibited triglyceridesecretion. ADRP overexpression also resulted in accumulation of triglycerides and decreasedtriglyceride secretion. The decreased secretion was not due to lack of triglycerides. Rather,PPARalpha activation prevents the availability of cytosolic triglycerides for VLDL assembly, inpart by increasing the expression of ADRP. Hepatic overexpression of PGC-1beta in miceinduced a hyperlipidemic response with a marked increase in apoB-containing lipoproteins.The hyperlipidemia was associated with increased diacylglycerol acyltransferase (DGAT)-1expression and plasma free fatty acids. The potentially beneficial effects of Wy on genescontrolling lipid metabolism were blunted by PGC-1beta overexpression.In summary, high GH levels are associated with increased atherosclerosis and hepatic VLDLsecretion. A few hepatic GH effects are dependent on PPARalpha. PPARalpha activation decreaseshepatic VLDL secretion by compartmentalization of intracellular triglycerides and hepaticPGC-1beta overexpression results in combined hyperlipidemia and decreased PPARalphasignaling.

Subjects/Keywords: growth hormone; PPARalpha; atherosclerosis; lipid metabolism; fatty acids; apoB;

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APA (6^th Edition):

Ljungberg, A. 1. (2006). The role of PPARalpha and growth hormone in hepatic lipid metaboism and atherosclerosis. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/16865

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ljungberg, Anna 1977-. “The role of PPARalpha and growth hormone in hepatic lipid metaboism and atherosclerosis.” 2006. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed January 22, 2021. http://hdl.handle.net/2077/16865.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ljungberg, Anna 1977-. “The role of PPARalpha and growth hormone in hepatic lipid metaboism and atherosclerosis.” 2006. Web. 22 Jan 2021.

Vancouver:

Ljungberg A1. The role of PPARalpha and growth hormone in hepatic lipid metaboism and atherosclerosis. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2006. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/2077/16865.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ljungberg A1. The role of PPARalpha and growth hormone in hepatic lipid metaboism and atherosclerosis. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2006. Available from: http://hdl.handle.net/2077/16865

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

23. Valli, Haseeb. Atrial arrhythmogenesis in a murine model of mitochondrial insufficiency.

Degree: PhD, 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/294568

► Age-related atrial arrhythmias including atrial fibrillation are frequently encountered in clinical practice and are associated with significant mortality and morbidity. A putative role for chronic… (more)

▼ Age-related atrial arrhythmias including atrial fibrillation are frequently encountered in clinical practice and are associated with significant mortality and morbidity. A putative role for chronic mitochondrial impairment in their pathogenesis was investigated using a murine model with homozygous deficiency of the transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator-1 β (Pgc-1β-/-). Pgc-1β regulates mitochondrial biogenesis and function, and unlike other murine models of mitochondrial dysfunction Pgc-1β-/- mice have a mild cardiac phenotype, devoid of confounding contractile dysfunction. All experiments were performed in young (12-16 weeks) and aged (>52 weeks) Pgc-1β-/- mice and compared to aged-matched wild type (WT) controls. Sharp microelectrode recordings of cellular action potentials (AP) in a whole-heart Langendorff-perfused system revealed that the Pgc-1β-/- genotype was associated with an atrial arrhythmic phenotype that progressed with age. Young and aged Pgc-1β-/- hearts showed evidence of slowed AP conduction at the cellular level, through deficits in maximum rates of AP depolarization (dV/dt)max, and at the tissue level through prolonged AP latencies. Action potential duration (APD) was also significantly shorter in Pgc-1β-/- hearts at high heart rates. APD restitution has been linked to the pathogenesis of ventricular fibrillation and more recently AF. However in the present work the incidence of alternans or steepness of the restitution curves did not correlate with arrhythmic tendency. Loose patch clamp measurements demonstrated that Pgc-1β−/− atria had significantly lower inward Na+ currents than that of WT preparations, correlating to the differences in (dV/dt)max values. No differences in delayed outward (K+) currents were evident. Morphometric analysis revealed that Pgc-1β deficiency was associated with accelerated fibrosis, with aged Pgc-1β-/- hearts displaying the greatest fibrotic change. The Pgc-1β-/- murine model of chronic mitochondrial impairment results in an age-related atrial arrhythmic phenotype through adverse electrical and structural remodelling producing an atrial substrate promoting AP reentry and arrhythmia persistence.

Subjects/Keywords: Atrial fibrillation; arrhythmia; mitochondrial; metabolic; peroxisome proliferator-activated receptor γ coactivator-1 β; Pgc-1β

…NRF-2 Nuclear respiratory factor-2 PES Programmed electrical stimulation PGC-1… …49 1.8 Peroxisome proliferator-activated receptor γ coactivator-1 family… …66 ii 3 Age-related electrocardiographic changes in Pgc-1β deficient murine hearts . 67… …69 3.3.2 Pgc-1β-/- hearts display impaired heart rate responses… …71 3.3.3 Aged-related SA node disease in WT and Pgc-1β-/- murine hearts…

10 more images…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Valli, H. (2019). Atrial arrhythmogenesis in a murine model of mitochondrial insufficiency. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/294568

Chicago Manual of Style (16^th Edition):

Valli, Haseeb. “Atrial arrhythmogenesis in a murine model of mitochondrial insufficiency.” 2019. Doctoral Dissertation, University of Cambridge. Accessed January 22, 2021. https://www.repository.cam.ac.uk/handle/1810/294568.

MLA Handbook (7^th Edition):

Valli, Haseeb. “Atrial arrhythmogenesis in a murine model of mitochondrial insufficiency.” 2019. Web. 22 Jan 2021.

Vancouver:

Valli H. Atrial arrhythmogenesis in a murine model of mitochondrial insufficiency. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Jan 22]. Available from: https://www.repository.cam.ac.uk/handle/1810/294568.

Council of Science Editors:

Valli H. Atrial arrhythmogenesis in a murine model of mitochondrial insufficiency. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/294568

24. SIVASUBRAMANIAN MEENALOCHANI. ROLE OF SPHK2/S1P SIGNALLING IN REGULATING MITOCHONDRIAL FUNCTION IN THE MPTP – INDUCED MOUSE MODEL OF PARKINSON’S DISEASE AND IN THE MPP+-TREATED MN9D CELLS.

Degree: 2014, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/118890

Subjects/Keywords: Parkinson’s disease; sphingosine kinase 2 (Sphk2); sphingosine-1-phosphate (S1P); Peroxisome proliferator-activated receptor γ coactivator 1α (PGC 1a)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

MEENALOCHANI, S. (2014). ROLE OF SPHK2/S1P SIGNALLING IN REGULATING MITOCHONDRIAL FUNCTION IN THE MPTP – INDUCED MOUSE MODEL OF PARKINSON’S DISEASE AND IN THE MPP+-TREATED MN9D CELLS. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/118890

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

MEENALOCHANI, SIVASUBRAMANIAN. “ROLE OF SPHK2/S1P SIGNALLING IN REGULATING MITOCHONDRIAL FUNCTION IN THE MPTP – INDUCED MOUSE MODEL OF PARKINSON’S DISEASE AND IN THE MPP+-TREATED MN9D CELLS.” 2014. Thesis, National University of Singapore. Accessed January 22, 2021. http://scholarbank.nus.edu.sg/handle/10635/118890.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

MEENALOCHANI, SIVASUBRAMANIAN. “ROLE OF SPHK2/S1P SIGNALLING IN REGULATING MITOCHONDRIAL FUNCTION IN THE MPTP – INDUCED MOUSE MODEL OF PARKINSON’S DISEASE AND IN THE MPP+-TREATED MN9D CELLS.” 2014. Web. 22 Jan 2021.

Vancouver:

MEENALOCHANI S. ROLE OF SPHK2/S1P SIGNALLING IN REGULATING MITOCHONDRIAL FUNCTION IN THE MPTP – INDUCED MOUSE MODEL OF PARKINSON’S DISEASE AND IN THE MPP+-TREATED MN9D CELLS. [Internet] [Thesis]. National University of Singapore; 2014. [cited 2021 Jan 22]. Available from: http://scholarbank.nus.edu.sg/handle/10635/118890.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

MEENALOCHANI S. ROLE OF SPHK2/S1P SIGNALLING IN REGULATING MITOCHONDRIAL FUNCTION IN THE MPTP – INDUCED MOUSE MODEL OF PARKINSON’S DISEASE AND IN THE MPP+-TREATED MN9D CELLS. [Thesis]. National University of Singapore; 2014. Available from: http://scholarbank.nus.edu.sg/handle/10635/118890

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

25. Attia, Ramy Naguib. Regulation of Pyruvate Dehydrogenase Kinase 4 by Thyroid Hormone / Role of Peroxisome Proliferator Activated Receptor Gamma Coactivator-1 alpha and Ccaat Enhancer Binding Protein.

Degree: PhD, Biomedical Sciences, 2009, University of Tennessee Health Science Center

URL: https://dc.uthsc.edu/dissertations/20

► Pyruvate dehydrogenase kinase 4 (PDK4) regulates pyruvate oxidation through the phosphorylation and inhibition of the pyruvate dehydrogenase complex (PDC). The PDC catalyzes the conversion… (more)

▼ Pyruvate dehydrogenase kinase 4 (PDK4) regulates pyruvate oxidation through the phosphorylation and inhibition of the pyruvate dehydrogenase complex (PDC). The PDC catalyzes the conversion of pyruvate to acetyl-CoA and it is an important control point in glucose and pyruvate metabolism. Previous studies had reported that PDK4 gene expression is induced by thyroid hormone (T3). These studies did not investigate the mechanisms by which T3 regulated PDK4 gene expression. I have examined the role of the thyroid hormone receptor (TR), transcriptional coactivators especially the peroxisome proliferator activated receptor gamma coactivator-1 (PGC-1α) and other transcription factors that act as accessory factors in T3 actions. Thyroid hormone receptors (TRα or TRβ) are part of the nuclear receptor family and have been implicated in the induction of many genes by T3. The nuclear receptors constitute a broad class of transcription factors that have the ability to bind to DNA and regulate the expression of the genes in a ligand dependent manner. To identify a binding site for the TRβ in the promoter of the PDK4 gene, I transfected serial deletions of this promoter ligated to the luciferase reporter gene into the human hepatoma (HepG2) cells. The TRβ binding site was characterized by gel shift mobility assays, site directed mutagenesis and in vivo and in vitro luciferase constructs transfection techniques. In addition, I have used the chromatin immunoprecipitation (ChIP) technique to confirm the binding of the TRβ to the PDK4 gene promoter. Transcription coregulators bind to nuclear receptors to facilitate or inhibit the transcription of the target genes. I have explored the role of several coregulators including the transcriptional coactivator peroxisome proliferator activated receptor gamma coactivator-1 (PGC-1α). Previous studies demonstrated that PGC-1α could induce the PDK4 gene. Here, I found that T3 increases PGC-1α abundance and association with the PDK4 gene. In addition, adenoviral shRNA-mediated knock-down of PGC-1α reduced the T3 induction of PDK4 and several other genes. These data suggest that PGC-1α participates in the T3 induction of multiple genes in the liver. In addition, I investigated the role of several transcription factors including estrogen related receptor (ERRα), CCAAT/enhancer binding protein beta (C/EBPß) and the forkhead transcription factor (FOXO1) in the activation of the PDK4 gene by T3. ERRα and FoxO1 recruit PGC-1α to the proximal PDK4 promoter and are involved in the synergistic stimulation of the PDK4 gene by T3 and PGC-1α. C/EBPß was identified as an important accessory factor in the T3 induction of the PDK4 gene. Knock-down of C/EBPß with adenoviral shRNA decreased both the basal expression and T3 stimulation of PDK4. Overall, my results showed that T3 induces PDK4 gene expression through a TRβ binding site in the promoter of the PDK4 gene and that the two transcription coregulators PGC-1α and C/EBPβ enhance this induction. Finally, I have tested… Advisors/Committee Members: Edwards A. Park, Ph.D..

Subjects/Keywords: C/EBP beta; PGC-1 alpha; Pyruvate dehydrogenase kinase 4; Thyroid hormone; Medical Biochemistry; Medical Cell Biology; Medicine and Health Sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Attia, R. N. (2009). Regulation of Pyruvate Dehydrogenase Kinase 4 by Thyroid Hormone / Role of Peroxisome Proliferator Activated Receptor Gamma Coactivator-1 alpha and Ccaat Enhancer Binding Protein. (Doctoral Dissertation). University of Tennessee Health Science Center. Retrieved from https://dc.uthsc.edu/dissertations/20

Chicago Manual of Style (16^th Edition):

Attia, Ramy Naguib. “Regulation of Pyruvate Dehydrogenase Kinase 4 by Thyroid Hormone / Role of Peroxisome Proliferator Activated Receptor Gamma Coactivator-1 alpha and Ccaat Enhancer Binding Protein.” 2009. Doctoral Dissertation, University of Tennessee Health Science Center. Accessed January 22, 2021. https://dc.uthsc.edu/dissertations/20.

MLA Handbook (7^th Edition):

Attia, Ramy Naguib. “Regulation of Pyruvate Dehydrogenase Kinase 4 by Thyroid Hormone / Role of Peroxisome Proliferator Activated Receptor Gamma Coactivator-1 alpha and Ccaat Enhancer Binding Protein.” 2009. Web. 22 Jan 2021.

Vancouver:

Attia RN. Regulation of Pyruvate Dehydrogenase Kinase 4 by Thyroid Hormone / Role of Peroxisome Proliferator Activated Receptor Gamma Coactivator-1 alpha and Ccaat Enhancer Binding Protein. [Internet] [Doctoral dissertation]. University of Tennessee Health Science Center; 2009. [cited 2021 Jan 22]. Available from: https://dc.uthsc.edu/dissertations/20.

Council of Science Editors:

Attia RN. Regulation of Pyruvate Dehydrogenase Kinase 4 by Thyroid Hormone / Role of Peroxisome Proliferator Activated Receptor Gamma Coactivator-1 alpha and Ccaat Enhancer Binding Protein. [Doctoral Dissertation]. University of Tennessee Health Science Center; 2009. Available from: https://dc.uthsc.edu/dissertations/20

Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)

26. Πεΐδης, Φίλιππος. Μελέτη του βιολογικού ρόλου και των μοριακών αλληλεπιδράσεων μιας νέας οικογένειας πρωτεϊνικών κινασών που φωσφορυλιώνουν επαναλαμβανόμενες αλληλουχίες αργινίνης-σερίνης.

Degree: 2006, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)

URL: http://hdl.handle.net/10442/hedi/20056

► Serine/arginine protein kinases (SRPKs) represent a novel class of enzymes that specifically modify SR or RS dipeptide motifs. In the present thesis we studied the… (more)

▼ Serine/arginine protein kinases (SRPKs) represent a novel class of enzymes that specifically modify SR or RS dipeptide motifs. In the present thesis we studied the biological role and molecular interactions of a new member of the SRPK family, named SRPK1a. SRPK1a is an alternatively spliced form of SRPK1 and contains an insertion of 171 amino acids at its NH2-terminal domain. This additional sequence of SRPK1a contains a relatively high number of proline residues and two LXXLL motifs (148LAPLL152 and 158LGRLL162), which are thought to facilitate the interaction of different proteins with nuclear receptors. Using the yeast two-hybrid assay, we found that the extended NH2-terminal domain of SRPK1a interacts with the p53 tumor suppressor protein and with Scaffold Attachment Factor-B1, a nuclear scaffold-associated protein that interacts with specific DNA sequences, designated as Matrix Attachment Regions (MARs). Confirmation of the first interaction (SRPK1a with p53) was provided by in vitro pull-down assays, while the second interaction (SRPK1a with SAF-B1) was confirmed by in vitro binding assays, as well as by co-immunoprecipitation from 293T cells doubly transfected with SRPK1a and SAF-B1. Since SAF-B1 and p53 do not contain any RS dipeptides and therefore are not phosphorylated by SRPK1a, we searched for a new molecule linking SAF-B1, p53 and SRPK1a. Our research led us to the identification of P2P-R, a member of the proliferation potential proteins (P2P) that was previously shown to bind p53. P2P-R contains an RS domain that is targeted by SR protein kinases and especially by SRPK1a. Using GST-pulldown and co-immunoprecipitation assays we found that P2P-R also interacts, via its RS region, with SAF-B1. Moreover, both SAF-B1 and P2P-R were found to associate with the DNAse resistant nuclear matrix. In a following step, we showed that both SAF-B1 and P2P-R act as co-repressors of estrogen induced transcription and function as part of the estrogen receptor transcription complex together with estrogen receptor α, steroid receptor co-activator 1 (SRC-1) and co-activator associated arginine methyltransferase (CARM1). Using deletion analysis we found that the repressional activity of P2P-R is confined to its C-terminal most segment (amino acids 1314-1516). Furthermore, using differential cell extraction procedures, we showed that addition of the ERα ligand, estradiol or its antagonist tamoxifen, results in the translocation of a significant part of the receptor to the nuclear matrix fraction. This translocaton coincides with a raise in SR protein kinase activity in the same fraction. Most notably, SRPK1a positively influences estrogen induced transcription. Taken together our observations suggest that nuclear matrix entities influence estrogen-dependent transcription and SRPK1a may modulate the interactions among the components of the estrogen receptor regulatory complex and/or the nuclear matrix, in a manner that leads to transcriptional activation. In addition, we performed studies in HepG2 cells, in…

Subjects/Keywords: Πυρηνική μήτρα; Πρωτεϊνικές κινάσες σερίνης-αργινίνης; Έλεγχος μεταγραφής; SRPK; p53; PZP-R; SAF-B (scaffold attachment factor); HNF4; ERa; PGC-1; Nuclear matrix

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Πεΐδης, . �. (2006). Μελέτη του βιολογικού ρόλου και των μοριακών αλληλεπιδράσεων μιας νέας οικογένειας πρωτεϊνικών κινασών που φωσφορυλιώνουν επαναλαμβανόμενες αλληλουχίες αργινίνης-σερίνης. (Thesis). Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Retrieved from http://hdl.handle.net/10442/hedi/20056

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Πεΐδης, Φίλιππος. “Μελέτη του βιολογικού ρόλου και των μοριακών αλληλεπιδράσεων μιας νέας οικογένειας πρωτεϊνικών κινασών που φωσφορυλιώνουν επαναλαμβανόμενες αλληλουχίες αργινίνης-σερίνης.” 2006. Thesis, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Accessed January 22, 2021. http://hdl.handle.net/10442/hedi/20056.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Πεΐδης, Φίλιππος. “Μελέτη του βιολογικού ρόλου και των μοριακών αλληλεπιδράσεων μιας νέας οικογένειας πρωτεϊνικών κινασών που φωσφορυλιώνουν επαναλαμβανόμενες αλληλουχίες αργινίνης-σερίνης.” 2006. Web. 22 Jan 2021.

Vancouver:

Πεΐδης �. Μελέτη του βιολογικού ρόλου και των μοριακών αλληλεπιδράσεων μιας νέας οικογένειας πρωτεϊνικών κινασών που φωσφορυλιώνουν επαναλαμβανόμενες αλληλουχίες αργινίνης-σερίνης. [Internet] [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2006. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10442/hedi/20056.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Πεΐδης �. Μελέτη του βιολογικού ρόλου και των μοριακών αλληλεπιδράσεων μιας νέας οικογένειας πρωτεϊνικών κινασών που φωσφορυλιώνουν επαναλαμβανόμενες αλληλουχίες αργινίνης-σερίνης. [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2006. Available from: http://hdl.handle.net/10442/hedi/20056

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Université de Montréal

27. Rodrigue-Way, Amélie. Regulation of lipid metabolism in adipocytes and hepatocytes by hexarelin through scavenger receptor CD36.

Degree: 2011, Université de Montréal

URL: http://hdl.handle.net/1866/5998

Subjects/Keywords: CD36; Hexarelin; PPARgamma; PGC-1alpha; Mitochondrial biogenesis; UCP-1; Fatty acid oxidation; AMPK; HMG-CoA Reductase; Insig-2; Hexaréline; Biogenèse mitochondriale; Oxydation des acides gras; Erk; Adipocytes; Hépatocytes; LKB1; Biology - Molecular / Biologie - Biologie moléculaire (UMI : 0307)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Rodrigue-Way, A. (2011). Regulation of lipid metabolism in adipocytes and hepatocytes by hexarelin through scavenger receptor CD36. (Thesis). Université de Montréal. Retrieved from http://hdl.handle.net/1866/5998

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Rodrigue-Way, Amélie. “Regulation of lipid metabolism in adipocytes and hepatocytes by hexarelin through scavenger receptor CD36.” 2011. Thesis, Université de Montréal. Accessed January 22, 2021. http://hdl.handle.net/1866/5998.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Rodrigue-Way, Amélie. “Regulation of lipid metabolism in adipocytes and hepatocytes by hexarelin through scavenger receptor CD36.” 2011. Web. 22 Jan 2021.

Vancouver:

Rodrigue-Way A. Regulation of lipid metabolism in adipocytes and hepatocytes by hexarelin through scavenger receptor CD36. [Internet] [Thesis]. Université de Montréal; 2011. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1866/5998.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Rodrigue-Way A. Regulation of lipid metabolism in adipocytes and hepatocytes by hexarelin through scavenger receptor CD36. [Thesis]. Université de Montréal; 2011. Available from: http://hdl.handle.net/1866/5998

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

28. Zhang, Yunyan. Roles of PGC-1α/PPARs pathway in regulating insulin sensitivity in mouse skeletal muscle cells under prolonged hypoxia.

Degree: 2012, University of Western Ontario

URL: https://ir.lib.uwo.ca/etd/998

► Using the C2C12 mouse myoblast cell line, I investigated how prolonged hypoxia affected components of the insulin signalling and FAO/PGC-1α/PPARs pathways, as they might impact… (more)

Subjects/Keywords: Intrauterine growth restriction (IUGR); hypoxia; fatty acid β-oxidation (FAO); insulin resistance; insulin signaling pathway; peroxisome proliferator-activated receptor (PPAR); PPAR- γ coactivator 1-α (PGC-1α); silent information regulator T1 (SIRT1); Medical Physiology

…post translational modification is also important to its activation. Deacetylation of PGC-1 α… …Roles of prolonged hypoxia on altering PGC-1α/PPARs interactions .......... 50 4.4 Activation… …14 Figure 1.2: Illustration of the FAO/PGC-1α/PPARs interactions… …34 Figure 3.7: Reduced oxygen tension did not affect PGC-1α mRNA, but did affect protein… …37 Figure 3.8: Reduced oxygen tension increased acetylated PGC-1α protein…

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APA (6^th Edition):

Zhang, Y. (2012). Roles of PGC-1α/PPARs pathway in regulating insulin sensitivity in mouse skeletal muscle cells under prolonged hypoxia. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/998

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Zhang, Yunyan. “Roles of PGC-1α/PPARs pathway in regulating insulin sensitivity in mouse skeletal muscle cells under prolonged hypoxia.” 2012. Thesis, University of Western Ontario. Accessed January 22, 2021. https://ir.lib.uwo.ca/etd/998.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Zhang, Yunyan. “Roles of PGC-1α/PPARs pathway in regulating insulin sensitivity in mouse skeletal muscle cells under prolonged hypoxia.” 2012. Web. 22 Jan 2021.

Vancouver:

Zhang Y. Roles of PGC-1α/PPARs pathway in regulating insulin sensitivity in mouse skeletal muscle cells under prolonged hypoxia. [Internet] [Thesis]. University of Western Ontario; 2012. [cited 2021 Jan 22]. Available from: https://ir.lib.uwo.ca/etd/998.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Zhang Y. Roles of PGC-1α/PPARs pathway in regulating insulin sensitivity in mouse skeletal muscle cells under prolonged hypoxia. [Thesis]. University of Western Ontario; 2012. Available from: https://ir.lib.uwo.ca/etd/998

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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