subject:(Proopiomelanocortin)

University of Hong Kong

1. Cheng, Kwai-wa. Molecular studies of proopiomelanocortin in goldfish brain.

Degree: 1996, University of Hong Kong

URL: http://hdl.handle.net/10722/32918

Subjects/Keywords: Proopiomelanocortin.; Goldfish.

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Cheng, K. (1996). Molecular studies of proopiomelanocortin in goldfish brain. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/32918

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):

Cheng, Kwai-wa. “Molecular studies of proopiomelanocortin in goldfish brain.” 1996. Thesis, University of Hong Kong. Accessed April 11, 2021. http://hdl.handle.net/10722/32918.

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

MLA Handbook (7^th Edition):

Cheng, Kwai-wa. “Molecular studies of proopiomelanocortin in goldfish brain.” 1996. Web. 11 Apr 2021.

Vancouver:

Cheng K. Molecular studies of proopiomelanocortin in goldfish brain. [Internet] [Thesis]. University of Hong Kong; 1996. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/10722/32918.

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

Council of Science Editors:

Cheng K. Molecular studies of proopiomelanocortin in goldfish brain. [Thesis]. University of Hong Kong; 1996. Available from: http://hdl.handle.net/10722/32918

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

NSYSU

2. Kuo, Yu-Fen. POMC Overexpression Stimulates MITF/HIF-1Î± Survival Pathway in B16-F10 Melanoma Cells.

Degree: Master, Biological Sciences, 2008, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0901108-100731

► Melanoma is a cancer of the pigment producing cells, melanocytes, and is the most serious type of skin cancer. Cancer is a condition in which… (more)

▼ Melanoma is a cancer of the pigment producing cells, melanocytes, and is the most serious type of skin cancer. Cancer is a condition in which one type of cell grows without limit in a disorganized fashion, disrupting and replacing normal tissues and their functions. Normal melanocytes reside in the outer layer of the skin and produce a brown pigment called melanin, which is responsible for skin color. Melanoma occurs when melanocytes become cancerous, grow, and invade other tissues. Pro-opiomelanocortin (POMC) is a precursor polypeptide of 241 amino acids and the prohormone of various neuropeptide, including corticotropin (ACTH), Î±-melanocyte-stimulating hormone (Î±-MSH), and Î²-endorphin (Î²-EP). Recently, we demonstrated that systemic POMC overexpression potently suppresses the growth and metastasis of B16-F10 melanoma in vitro and in vivo. However, despite potent inhibition of tumor proliferation and angiogenesis, B16-F10 melanoma still managed to survive after POMC gene therapy. The underlying survival mechanism of B16-F10 melanoma remains unclear. Microphthalmia-associated transcription factor (MITF) is a basic helix-loop-helix transcription factor that plays a key role not only in melanin synthesis, but also in melanocyte development and survival. Besides, MITF binds to the hypoxia-inducible factor-1Î± (HIF-1Î±) promoter to stimulate its transcriptional activity. In this study, we investigate the influence of POMC gene delivery on the pro-survival MITF/HIF-1Î± pathway in B16-F10 melanoma cells. Quantitative RT-PCR and western blot analysis revealed that POMC gene delivery increased the MITF mRNA and protein level in B16-F10 melanoma cells. Besides, POMC gene delivery significantly enhanced the HIF-1Î±-driven luciferase activities in melanoma cells. By transfection and puromycin selection, we generated and characterized a MITF-knockdown B16-F10 melanoma cells (MITF KD) stably expressing short hairpin RNA against MITF. The growth, invasion, and colonies formation of MITF-KD were similar to those of vector control. However, implantation of MITF-KD cells led to melanoma with significantly reduced tumor size compared with those in mice implanted with vector control cells. Histological analysis revealed a significant reduction of CD31-positive blood vessels in implantation of MITF-KD cells-treated tumors, which was accompanied with a decrease in Ki-67-positive proliferating cells and an increase in TUNEL-positive apoptotic cells. Moreover, POMC-mediated upregulation of MITF and HIF-1 Î± was significantly attenuated in MITF KD-B16-F10 cells. Acetylsalicylic acid (aspirin; ASA) is widely used as an analgesic/antipyretic drug. ASA exhibits a wide range of biological effects, including preventative effects against heart attack, stroke, and the development of some types of cancer. In our study, we found ASA enhanced cell proliferation. However, in invasion test, ASA had no effect on cell migration. POMC gene delivery elevated the mRNA and protein level of hemeoxygenase-1 (HO-1), a downstream effector of HIF-1Î± pathway… Advisors/Committee Members: Ming-Hong Tai (committee member), Cheng, Jiin-Tsuey (chair), HONG YI-REN (chair).

Subjects/Keywords: Heme oxygenase-1; Adenovirus; Proopiomelanocortin; melanoma

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Kuo, Y. (2008). POMC Overexpression Stimulates MITF/HIF-1Î± Survival Pathway in B16-F10 Melanoma Cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0901108-100731

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):

Kuo, Yu-Fen. “POMC Overexpression Stimulates MITF/HIF-1Î± Survival Pathway in B16-F10 Melanoma Cells.” 2008. Thesis, NSYSU. Accessed April 11, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0901108-100731.

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

MLA Handbook (7^th Edition):

Kuo, Yu-Fen. “POMC Overexpression Stimulates MITF/HIF-1Î± Survival Pathway in B16-F10 Melanoma Cells.” 2008. Web. 11 Apr 2021.

Vancouver:

Kuo Y. POMC Overexpression Stimulates MITF/HIF-1Î± Survival Pathway in B16-F10 Melanoma Cells. [Internet] [Thesis]. NSYSU; 2008. [cited 2021 Apr 11]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0901108-100731.

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

Council of Science Editors:

Kuo Y. POMC Overexpression Stimulates MITF/HIF-1Î± Survival Pathway in B16-F10 Melanoma Cells. [Thesis]. NSYSU; 2008. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0901108-100731

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

3. Benchekroun, Ghita. Caractérisation morphologique et fonctionnelle des tumeurs corticotropes du chien et du chat : Functional and morphological characterization of corticotropic tumors in dogs and cats.

Degree: Docteur es, Pathologie et recherche clinique, 2016, Université Paris-Est

URL: http://www.theses.fr/2016PESC0070

►

La maladie de Cushing résulte du développement de tumeurs hypophysaires corticotropes d’agressivité variable. Cette forme d'hypercorticisme dépendante de l’ACTH se distingue des formes indépendantes de… (more)

▼

La maladie de Cushing résulte du développement de tumeurs hypophysaires corticotropes d’agressivité variable. Cette forme d'hypercorticisme dépendante de l’ACTH se distingue des formes indépendantes de l’ACTH, souvent consécutives à une tumeur surrénalienne. Les outils de distinction entre ces deux formes ainsi que les marqueurs d’agressivité des tumeurs hypophysaires ont été peu documentés ; ils seraient pourtant précieux pour les cliniciens. Un premier objectif, atteint, de notre travail a visé à identifier sur des cohortes cliniquement caractérisées de chiens atteints de syndrome de Cushing, des marqueurs sanguins et morphologiques qui soient distinctifs des deux formes de syndromes de Cushing (concentration plasmatique en ACTH, échographie et examen tomodensitométrique des glandes surrénales). Un second objectif de notre travail a visé à identifier des paramètres cliniques et biologiques susceptibles de refléter l'agressivité des tumeurs corticotropes. Nous avons ainsi montré chez le chien qu'une hypothermie ou une bradycardie peut signer une tumeur de grande taille. Chez le chat, atteint d'adénomes corticotropes généralement agressifs, nous avons démontré que le dosage de la POMC plasmatique est pertinent pour diagnostiquer la maladie de Cushing. La valeur élevée de la concentration plasmatique en POMC chez l'homme, le chien et le chat, a suggéré que ces tumeurs induisent un défaut de maturation de la POMC. L'analyse par western-blot des acteurs protéiques de cette maturation chez le chien a en effet révélé une diminution de la quantité d'enzyme pro-convertase 1/3 au sein des tumeurs corticotropes de grande taille.

Cushing’s disease or hyperadrenocorticism (HAC) is one of the most frequent endocrine diseases in dogs. Most cases are ACTH-dependent HAC and are associated with pituitary tumors of variable aggressiveness. The other form of HAC is known as ACTH-independent. The present work was carried out on cohort of dogs and cats presented with HAC. The first objective of this work was to assess the accuracy of diagnostic investigations (such as adrenal glands ultrasonography, computed tomodensitometry scan of adrenal glands and pituitary gland and basal ACTH measurement) in a large cohort of dogs with HAC and to identify the best thresholds that allow a correct classification of HAC (ACTH dependent vs ACTH independent). The second objective was to demonstrate that clinical information such as bradycardia or hypothermia reflect the aggressiveness of the pituitary tumor. We also demonstrated that plasma proopiomelanocortin (POMC) concentration was elevated in cats with Cushing’s disease. This observation, previously reported in dogs and humans, suggests a physiopathological implication of ACTH loss of maturation in aggressive pituitary tumour. We investigated if proconvertase 1/3 (PC1/3) could be involved in this alteration through western blot detection of POMC, pro-ACTH, ACTH and PC1/3 in corticotropic tumors. This work showed a difference in PC1/3 protein levels between large and small corticotroph tumours,…

Advisors/Committee Members: Tiret, Laurent (thesis director), Rosenberg, Dan (thesis director).

Subjects/Keywords: Corticotrope; Tumeur; Endocrinologie; Proopiomelanocortin; Hormone corticotrope; Proconvertase 1/3; Corticotropic; Tumor; Endocrine disease; Proopiomelanocortin; Acth; Proconvertase 1/3; 630

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Benchekroun, G. (2016). Caractérisation morphologique et fonctionnelle des tumeurs corticotropes du chien et du chat : Functional and morphological characterization of corticotropic tumors in dogs and cats. (Doctoral Dissertation). Université Paris-Est. Retrieved from http://www.theses.fr/2016PESC0070

Chicago Manual of Style (16^th Edition):

Benchekroun, Ghita. “Caractérisation morphologique et fonctionnelle des tumeurs corticotropes du chien et du chat : Functional and morphological characterization of corticotropic tumors in dogs and cats.” 2016. Doctoral Dissertation, Université Paris-Est. Accessed April 11, 2021. http://www.theses.fr/2016PESC0070.

MLA Handbook (7^th Edition):

Benchekroun, Ghita. “Caractérisation morphologique et fonctionnelle des tumeurs corticotropes du chien et du chat : Functional and morphological characterization of corticotropic tumors in dogs and cats.” 2016. Web. 11 Apr 2021.

Vancouver:

Benchekroun G. Caractérisation morphologique et fonctionnelle des tumeurs corticotropes du chien et du chat : Functional and morphological characterization of corticotropic tumors in dogs and cats. [Internet] [Doctoral dissertation]. Université Paris-Est; 2016. [cited 2021 Apr 11]. Available from: http://www.theses.fr/2016PESC0070.

Council of Science Editors:

Benchekroun G. Caractérisation morphologique et fonctionnelle des tumeurs corticotropes du chien et du chat : Functional and morphological characterization of corticotropic tumors in dogs and cats. [Doctoral Dissertation]. Université Paris-Est; 2016. Available from: http://www.theses.fr/2016PESC0070

4. Bruna Morais Faleiros de Paula. Padrões de metilação e expressão do gene Pomc na prole de ratas submetidas às dietas deficiente e suplementada com ácido fólico.

Degree: 2016, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/17/17138/tde-30032017-093539/

►

A epigenética é uma subárea da Genética, na qual são estudados mecanismos que são essenciais para o adequado desenvolvimento dos mamíferos, sendo que, alterações neste… (more)

▼

A epigenética é uma subárea da Genética, na qual são estudados mecanismos que são essenciais para o adequado desenvolvimento dos mamíferos, sendo que, alterações neste estágio podem levar a vários distúrbios metabólicos, como a obesidade. Atualmente a obesidade é um grave problema de saúde pública mundial, tem origem multifatorial envolvendo tanto fatores ambientais quanto genéticos. Existem alguns genes que estão envolvidos com a obesidade, como por exemplo, o gene da pró-opiomelanocortina (POMC). O objetivo do presente projeto de pesquisa é investigar os padrões de expressão e metilação do gene Pomc na prole de ratas submetidas às dietas deficiente e suplementada com ácido fólico. Os animais utilizados foram ratos Wistar. O estudo envolveu filhotes (n=24) machos e fêmeas que foram desmamados com a mesma dieta de suas respectivas mães, sendo três grupos de tratamento, o grupo controle (2,0 mg de ácido fólico/kg de ração), o grupo deficiente (0,5 mg de ácido fólico/kg de ração) e o grupo suplementado (8 mg de ácido fólico/kg de ração). Foram coletadas amostras do núcleo arqueado do hipotálamo, a partir das quais foram extraídos DNA, RNA e proteínas utilizando kits comerciais seguindo o protocolo do fabricante. Com o DNA foi realizada a análise do padrão de metilação. O mRNA foi utilizado para a análise da expressão gênica, por PCR em tempo real, pelo sistema TaqMan® (Life Technologies(TM)). O estudo de proteômica foi realizado por Western blotting. De modo geral, observou-se que o peso corpóreo dos filhotes machos não apresentou diferença estatística entre os grupos. O consumo de ração do grupo deficiente em ácido fólico foi estatisticamente (p = 0,03) maior do que o grupo controle. Em relação aos filhotes fêmeas observou-se que o peso corpóreo do grupo suplementado foi estatisticamente (p = 0,01) maior do que o grupo controle, e referente ao consumo de ração, não houve diferença estatística significativa entre os grupos de tratamento. As análises de peso cerebral, expressão gênica, metilação e expressão proteica de Pomc não apresentaram diferenças estatísticas significativas entre os grupos de tratamento de ambos os sexos. Conclui-se que a intervenção com dietas com diferentes concentrações de ácido fólico não ocasionou alterações significativas na prole, em relação ao estudo de proteômica e aos padrões de metilação e expressão do gene Pomc. Quanto ao peso corpóreo e consumo de ração dos animais mostrou-se que a suplementação com ácido fólico durante a gestação e no pós desmame foi capaz de alterar estes dois parâmetros, com resposta divergente entre os machos e fêmeas na prole adulta.

Epigenetic mechanisms are essential for proper development in mammals, and that changes at this stage may lead to various metabolic disorders such as obesity. Currently obesity is a serious problem of public health worldwide, has a multifactorial origin involving both environmental and genetic factors. There are some genes that are involved with obesity, such as the proopiomelanocortin gene (POMC). The aim of this research…

Advisors/Committee Members: Helio Vannucchi, Carla Barbosa Nonino, Sérgio Alberto Rupp de Paiva.

Subjects/Keywords: Ácido Fólico; Epigenética; Metilação; Proopiomelanocortina; Epigenetic; Folic Acid; Methylation; Proopiomelanocortin

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Paula, B. M. F. d. (2016). Padrões de metilação e expressão do gene Pomc na prole de ratas submetidas às dietas deficiente e suplementada com ácido fólico. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/17/17138/tde-30032017-093539/

Chicago Manual of Style (16^th Edition):

Paula, Bruna Morais Faleiros de. “Padrões de metilação e expressão do gene Pomc na prole de ratas submetidas às dietas deficiente e suplementada com ácido fólico.” 2016. Masters Thesis, University of São Paulo. Accessed April 11, 2021. http://www.teses.usp.br/teses/disponiveis/17/17138/tde-30032017-093539/.

MLA Handbook (7^th Edition):

Paula, Bruna Morais Faleiros de. “Padrões de metilação e expressão do gene Pomc na prole de ratas submetidas às dietas deficiente e suplementada com ácido fólico.” 2016. Web. 11 Apr 2021.

Vancouver:

Paula BMFd. Padrões de metilação e expressão do gene Pomc na prole de ratas submetidas às dietas deficiente e suplementada com ácido fólico. [Internet] [Masters thesis]. University of São Paulo; 2016. [cited 2021 Apr 11]. Available from: http://www.teses.usp.br/teses/disponiveis/17/17138/tde-30032017-093539/.

Council of Science Editors:

Paula BMFd. Padrões de metilação e expressão do gene Pomc na prole de ratas submetidas às dietas deficiente e suplementada com ácido fólico. [Masters Thesis]. University of São Paulo; 2016. Available from: http://www.teses.usp.br/teses/disponiveis/17/17138/tde-30032017-093539/

Freie Universität Berlin

5. Kühnen, Peter. Epigenetic and genetic causes for obesity and impaired insulin secretion and new diagnostic- and therapeutic options.

Degree: 2018, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-7919

► Obesity and diseases with impaired insulin secretion (congenital hyperinsulinism, diabetes mellitus) are important endocrine disorders. Here, an epigenetic variant within the POMC gene as a… (more)

Subjects/Keywords: Obesity; Epigenetics; Proopiomelanocortin; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Kühnen, P. (2018). Epigenetic and genetic causes for obesity and impaired insulin secretion and new diagnostic- and therapeutic options. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-7919

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):

Kühnen, Peter. “Epigenetic and genetic causes for obesity and impaired insulin secretion and new diagnostic- and therapeutic options.” 2018. Thesis, Freie Universität Berlin. Accessed April 11, 2021. http://dx.doi.org/10.17169/refubium-7919.

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

MLA Handbook (7^th Edition):

Kühnen, Peter. “Epigenetic and genetic causes for obesity and impaired insulin secretion and new diagnostic- and therapeutic options.” 2018. Web. 11 Apr 2021.

Vancouver:

Kühnen P. Epigenetic and genetic causes for obesity and impaired insulin secretion and new diagnostic- and therapeutic options. [Internet] [Thesis]. Freie Universität Berlin; 2018. [cited 2021 Apr 11]. Available from: http://dx.doi.org/10.17169/refubium-7919.

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

Council of Science Editors:

Kühnen P. Epigenetic and genetic causes for obesity and impaired insulin secretion and new diagnostic- and therapeutic options. [Thesis]. Freie Universität Berlin; 2018. Available from: http://dx.doi.org/10.17169/refubium-7919

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

6. LEE YUNG SENG. Elucidating the genetic basis of severe obesity: learning from the experiments of nature.

Degree: 2009, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/16681

Subjects/Keywords: obesity MC3R MC4R proopiomelanocortin gene mutation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

SENG, L. Y. (2009). Elucidating the genetic basis of severe obesity: learning from the experiments of nature. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/16681

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):

SENG, LEE YUNG. “Elucidating the genetic basis of severe obesity: learning from the experiments of nature.” 2009. Thesis, National University of Singapore. Accessed April 11, 2021. http://scholarbank.nus.edu.sg/handle/10635/16681.

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

MLA Handbook (7^th Edition):

SENG, LEE YUNG. “Elucidating the genetic basis of severe obesity: learning from the experiments of nature.” 2009. Web. 11 Apr 2021.

Vancouver:

SENG LY. Elucidating the genetic basis of severe obesity: learning from the experiments of nature. [Internet] [Thesis]. National University of Singapore; 2009. [cited 2021 Apr 11]. Available from: http://scholarbank.nus.edu.sg/handle/10635/16681.

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

Council of Science Editors:

SENG LY. Elucidating the genetic basis of severe obesity: learning from the experiments of nature. [Thesis]. National University of Singapore; 2009. Available from: http://scholarbank.nus.edu.sg/handle/10635/16681

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

Freie Universität Berlin

7. Wittrock-Staar, Manon Josephine. Hypothalamic proopiomelanocortin promoter methylation of neonatally overnourished rats.

Degree: 2012, Freie Universität Berlin

URL: https://refubium.fu-berlin.de/handle/fub188/13219

► Introduction: Environmental alterations during critical periods of early development have fundamental impact on the lifelong disease susceptibility of the organism. For example, intrauterine hyperglycemia or… (more)

▼ Introduction: Environmental alterations during critical periods of early development have fundamental impact on the lifelong disease susceptibility of the organism. For example, intrauterine hyperglycemia or rapid neonatal weight gain increase the risk of obesity und associated chronic diseases in adulthood. The most common epigenetic mechanism of these perinatal programming processes is the CpG-methylation of genes, which lead to permanent alterations in gene expression. It was postulated that neonatal overfeeding may alter DNA methylation pattern of the main anorectic neuropeptide in the hypothalamus proopiomelanocortin (POMC) and may cause permanent hyperphagia and metabolic disorders seen in these rats. Methods: Neonatal overfeeding was induced by rearing Wistar rats in small litters (SL). Using bisulfite sequencing DNA methylation status of the hypothalamic POMC gene promoter was mapped. POMC- mRNA-expression was measured by semiquantative RT-PCR. Results: Neonatal overfeeding led to rapid early weight gain, resulting in a metabolic syndrome phenotype: SL-rats presented obesity, hyperleptinemia, hyperglycemia, hyperinsulinemia, and an increased insulin/glucose ratio. In SL rats the hypothalamic gene promoter of the POMC showed hypermethylation of CpG dinucleotides within the binding sequences of transcription factors Sp1 and NF-kappaB. POMC expression lacked upregulation; moreover insulin- and leptin- related POMC-mRNA was significantly reduced in SL rats. DNA methylation within the Sp1 and NF-kappaB binding sequences was inversely correlated to the quotients of POMC expression/leptin and POMC expression/insulin. Glucose levels found to be significantly positively correlated to the CpG methylation of the POMC gene promoter and the binding sites of Sp1 and NF-kappaB. Conclusion: This is the first study to demonstrate binding-site specific epigenetic programming of hypothalamic POMC gene promoter by neonatal overfeeding in rats. Functional relevance of increased site-specific DNA methylation in SL rats was shown by lack of stimulation of POMC gene expression and inverse correlations. These findings reveal the neonatal period as critical for nutritional programming of a neuropeptide. Overfeeding and hyperglycemia seem to be epigenetic risk factors of obesity programming and consecutive metabolic syndrome. Advisors/Committee Members: [email protected] (contact), w (gender), Prof. Dr. med. A. Plagemann (firstReferee), Prof. Dr. med. J. Dötsch (furtherReferee), Prof. Dr. med. M. Zygmunt (furtherReferee).

Subjects/Keywords: obesity; perinatal programming; epigenomics; DNA methylation; hypothalamus; proopiomelanocortin (POMC); NF-kappaB.; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Wittrock-Staar, M. J. (2012). Hypothalamic proopiomelanocortin promoter methylation of neonatally overnourished rats. (Thesis). Freie Universität Berlin. Retrieved from https://refubium.fu-berlin.de/handle/fub188/13219

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):

Wittrock-Staar, Manon Josephine. “Hypothalamic proopiomelanocortin promoter methylation of neonatally overnourished rats.” 2012. Thesis, Freie Universität Berlin. Accessed April 11, 2021. https://refubium.fu-berlin.de/handle/fub188/13219.

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

MLA Handbook (7^th Edition):

Wittrock-Staar, Manon Josephine. “Hypothalamic proopiomelanocortin promoter methylation of neonatally overnourished rats.” 2012. Web. 11 Apr 2021.

Vancouver:

Wittrock-Staar MJ. Hypothalamic proopiomelanocortin promoter methylation of neonatally overnourished rats. [Internet] [Thesis]. Freie Universität Berlin; 2012. [cited 2021 Apr 11]. Available from: https://refubium.fu-berlin.de/handle/fub188/13219.

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

Council of Science Editors:

Wittrock-Staar MJ. Hypothalamic proopiomelanocortin promoter methylation of neonatally overnourished rats. [Thesis]. Freie Universität Berlin; 2012. Available from: https://refubium.fu-berlin.de/handle/fub188/13219

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

Freie Universität Berlin

8. Weiss, Deike. Neuroendocrine changes in patients with anorexia nevosa.

Degree: 2013, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-9570

► Patients with anorexia nervosa show neuroendocrine changes compared to healthy controls. It remains unclear, whether those are preexisting alterations or caused by the disease and… (more)

Subjects/Keywords: anorexia nervosa; preproenkephaline; ppE; proopiomelanocortin; POMC; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit::610 Medizin und Gesundheit

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Weiss, D. (2013). Neuroendocrine changes in patients with anorexia nevosa. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-9570

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):

Weiss, Deike. “Neuroendocrine changes in patients with anorexia nevosa.” 2013. Thesis, Freie Universität Berlin. Accessed April 11, 2021. http://dx.doi.org/10.17169/refubium-9570.

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

MLA Handbook (7^th Edition):

Weiss, Deike. “Neuroendocrine changes in patients with anorexia nevosa.” 2013. Web. 11 Apr 2021.

Vancouver:

Weiss D. Neuroendocrine changes in patients with anorexia nevosa. [Internet] [Thesis]. Freie Universität Berlin; 2013. [cited 2021 Apr 11]. Available from: http://dx.doi.org/10.17169/refubium-9570.

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

Council of Science Editors:

Weiss D. Neuroendocrine changes in patients with anorexia nevosa. [Thesis]. Freie Universität Berlin; 2013. Available from: http://dx.doi.org/10.17169/refubium-9570

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

9. Agapito, Maria. The role of Period 2 gene in mediating alcohol effects on metabolic signals in proopiomelanocortin producing neurons.

Degree: Neuroscience, 2013, Rutgers University

URL: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000068807

Subjects/Keywords: Proopiomelanocortin; Fetus – Metabolism; Fetal alcohol syndrome

…exposure on levels of proopiomelanocortin (Pomc) gene mRNA (A), β-endorphin… …proopiomelanocortin Pgc1α (aka PPARGC1A), Peroxisome proliferator-activated receptor gamma… …Nyomba’s lab concluded that perhaps ethanol disrupts the proopiomelanocortin system resulting in… …rhythm of proopiomelanocortin (POMC) mRNA expression and the circadian expression of…

10 more images…

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Agapito, M. (2013). The role of Period 2 gene in mediating alcohol effects on metabolic signals in proopiomelanocortin producing neurons. (Thesis). Rutgers University. Retrieved from http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000068807

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):

Agapito, Maria. “The role of Period 2 gene in mediating alcohol effects on metabolic signals in proopiomelanocortin producing neurons.” 2013. Thesis, Rutgers University. Accessed April 11, 2021. http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000068807.

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

MLA Handbook (7^th Edition):

Agapito, Maria. “The role of Period 2 gene in mediating alcohol effects on metabolic signals in proopiomelanocortin producing neurons.” 2013. Web. 11 Apr 2021.

Vancouver:

Agapito M. The role of Period 2 gene in mediating alcohol effects on metabolic signals in proopiomelanocortin producing neurons. [Internet] [Thesis]. Rutgers University; 2013. [cited 2021 Apr 11]. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000068807.

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

Council of Science Editors:

Agapito M. The role of Period 2 gene in mediating alcohol effects on metabolic signals in proopiomelanocortin producing neurons. [Thesis]. Rutgers University; 2013. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000068807

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

10. Zhang, Chao. Elucidation of the roles of agouti related proteins in zebrafish.

Degree: PhD, 2012, Oregon Health Sciences University

URL: doi:10.6083/M4FB50ZR ; http://digitalcommons.ohsu.edu/etd/755

Subjects/Keywords: Zebra danio; Proopiomelanocortin; MSH (Hormone); Agouti-Related Protein; Melanocortins; Zebrafish; Pro-Opiomelanocortin

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Zhang, C. (2012). Elucidation of the roles of agouti related proteins in zebrafish. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M4FB50ZR ; http://digitalcommons.ohsu.edu/etd/755

Chicago Manual of Style (16^th Edition):

Zhang, Chao. “Elucidation of the roles of agouti related proteins in zebrafish.” 2012. Doctoral Dissertation, Oregon Health Sciences University. Accessed April 11, 2021. doi:10.6083/M4FB50ZR ; http://digitalcommons.ohsu.edu/etd/755.

MLA Handbook (7^th Edition):

Zhang, Chao. “Elucidation of the roles of agouti related proteins in zebrafish.” 2012. Web. 11 Apr 2021.

Vancouver:

Zhang C. Elucidation of the roles of agouti related proteins in zebrafish. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 2012. [cited 2021 Apr 11]. Available from: doi:10.6083/M4FB50ZR ; http://digitalcommons.ohsu.edu/etd/755.

Council of Science Editors:

Zhang C. Elucidation of the roles of agouti related proteins in zebrafish. [Doctoral Dissertation]. Oregon Health Sciences University; 2012. Available from: doi:10.6083/M4FB50ZR ; http://digitalcommons.ohsu.edu/etd/755

University of Michigan

11. Morgan, Caurnel. Photoperiodic regulation of POMC systems in the golden hamster.

Degree: PhD, Neurosciences, 1996, University of Michigan

URL: http://hdl.handle.net/2027.42/129801

► In this dissertation, I investigated proopiomelanocortin (POMC) systems in the hypothalamus, testes, and anterior pituitary that are altered by switching the male golden hamster (Mesocricetus… (more)

▼ In this dissertation, I investigated proopiomelanocortin (POMC) systems in the hypothalamus, testes, and anterior pituitary that are altered by switching the male golden hamster (Mesocricetus auratus) from long photoperiods (LP) to short photoperiods (SP). I tested the following hypotheses: (1) SP stimulate POMC peptide secretion from the mediobasal hypothalamus (MBH); (2) SP inhibit POMC peptide secretion from the testes; (3) SP inhibit POMC peptide secretion from the anterior pituitary (AP); and (4) SP and agonistic encounters (i.e., social isolation followed by fighting) stimulate POMC peptide secretion from the AP. After exposure to SP (i.e., less than 12.5 hours of daily light), the hamster exhibits changes in the secretion of hormones regulating reproduction, metabolism, and social behavior, which are thought to be critical for winter survival. Although the underlying mechanisms are not completely understood, the POMC precursor, which encodes beta-endorphin (β-END) and adrenocorticotropic hormone (ACTH), may play a key role. The results show that the MBH β-END content, as assessed by radioimmunoassay (RIA), increases prior to the loss of testicular activity during SP. MBH β-END is thought to inhibit gonadal activity. In addition, increases followed by decreases in the testicular β-END content and POMC mRNA levels, as assessed by RIA and Northern analysis, suggest that testicular POMC is regulated by the photoperiod During SP, decreases in plasma ACTH and glucocorticoid levels, as assessed by RIA, are not temporally associated with decreases in the body fat content, even though the glucocorticoids are known to stimulate fat catabolism. In hamsters subjected to agonistic encounters and SP, increases in plasma ACTH and glucocorticoid levels are associated with pronounced increases in agonistic behavior. ACTH, via its stimulation of glucocorticoid secretion, is known to increase agonistic behavior. I conclude from these results that POMC peptides are involved in the photoperiodic regulation of gonadal and adrenal activities and possibly in the seasonal regulation of reproduction and social behavior, but not fat metabolism. Advisors/Committee Members: Akil, Huda (advisor), Karsch, Fred J. (advisor).

Subjects/Keywords: Golden; Hamster; Photoperiodic; Pomc; Proopiomelanocortin; Proopiomelanocortinreprod; Regulation; Reproduction; Social Behavior; Survival; Systems

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Morgan, C. (1996). Photoperiodic regulation of POMC systems in the golden hamster. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/129801

Chicago Manual of Style (16^th Edition):

Morgan, Caurnel. “Photoperiodic regulation of POMC systems in the golden hamster.” 1996. Doctoral Dissertation, University of Michigan. Accessed April 11, 2021. http://hdl.handle.net/2027.42/129801.

MLA Handbook (7^th Edition):

Morgan, Caurnel. “Photoperiodic regulation of POMC systems in the golden hamster.” 1996. Web. 11 Apr 2021.

Vancouver:

Morgan C. Photoperiodic regulation of POMC systems in the golden hamster. [Internet] [Doctoral dissertation]. University of Michigan; 1996. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/2027.42/129801.

Council of Science Editors:

Morgan C. Photoperiodic regulation of POMC systems in the golden hamster. [Doctoral Dissertation]. University of Michigan; 1996. Available from: http://hdl.handle.net/2027.42/129801

University of Michigan

12. Kelsey, Jeffrey Easton. Regulation Of Proopiomelanocortin Messenger-rna Levels And Translation (in Situ, Hybridization, Stress, Dot Blot, Pituitary).

Degree: PhD, Neurosciences, 1986, University of Michigan

URL: http://hdl.handle.net/2027.42/127914

► Proopiomelanocortin (POMC) is a large multipeptide precursor found in the anterior (AL) and intermediate lobes (IL) of the pituitary, the arcuate nucleus and the nucleus… (more)

▼ Proopiomelanocortin (POMC) is a large multipeptide precursor found in the anterior (AL) and intermediate lobes (IL) of the pituitary, the arcuate nucleus and the nucleus of the solitary tract. Secretion of POMC by pituitary cells is differentially regulated between the two lobes. The coordination of POMC mRNA levels with manipulations that alter release have been examined. Environmental stress, which produced parallel increases in POMC mRNA levels and plasma POMC peptides, was found to be a potent stimulator of both measures. Intermediate lobe melanotrophs were also found to respond to catecholaminergic stimuli by increasing POMC mRNA levels in response to dopamine antagonists and to beta-adrenergic agonists. These receptors were found to produce additive increases when ligands for both were administered together. A number of studies were performed to measure POMC translation/POMC mRNA levels and to determine if increased POMC mRNA levels were required to support increased POMC translation. Neither acute in vitro challenges or in vivo manipulations were effective in increasing POMC translational efficiency as a function of POMC mRNA. Two weeks of swim stress, which increased IL lobe POMC mRNA levels 3-fold, led to a decrease in translational efficiency, due perhaps to overloading of the ribosomes. In situ hybridization was performed to examine changes in POMC mRNA levels while retaining an anatomical context. Changes detected in IL POMC mRNA by in situ hybridization following administration of haloperidol paralleled those detected by blot hybridization. Resolution of single cells was also demonstrated in AL corticotrophs and in cells of the arcuate nucleus. These studies have demonstrated a coordination between POMC mRNA levels and secretory activity induced by environmental and pharmacological stimuli that are known to increase secretion of POMC peptides. This increase in POMC mRNA was shown in the IL to be necessary for increased translation of POMC which is required to replenish secreted peptides. This indicates that determination of mRNA levels can serve as an indicator of cellular response. In situ hybridization was shown to constitute a quantitative method for detecting changes in mRNA while retaining an anatomical context. This should prove useful in studying a heterogeneous tissue such as the brain.

Subjects/Keywords: Blot; Dot; Hybridization; Hybridizationstress; Levels; Messenger; Pituitary; Proopiomelanocortin; Regulation; Rna; Situ; Stress; Translation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Kelsey, J. E. (1986). Regulation Of Proopiomelanocortin Messenger-rna Levels And Translation (in Situ, Hybridization, Stress, Dot Blot, Pituitary). (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/127914

Chicago Manual of Style (16^th Edition):

Kelsey, Jeffrey Easton. “Regulation Of Proopiomelanocortin Messenger-rna Levels And Translation (in Situ, Hybridization, Stress, Dot Blot, Pituitary).” 1986. Doctoral Dissertation, University of Michigan. Accessed April 11, 2021. http://hdl.handle.net/2027.42/127914.

MLA Handbook (7^th Edition):

Kelsey, Jeffrey Easton. “Regulation Of Proopiomelanocortin Messenger-rna Levels And Translation (in Situ, Hybridization, Stress, Dot Blot, Pituitary).” 1986. Web. 11 Apr 2021.

Vancouver:

Kelsey JE. Regulation Of Proopiomelanocortin Messenger-rna Levels And Translation (in Situ, Hybridization, Stress, Dot Blot, Pituitary). [Internet] [Doctoral dissertation]. University of Michigan; 1986. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/2027.42/127914.

Council of Science Editors:

Kelsey JE. Regulation Of Proopiomelanocortin Messenger-rna Levels And Translation (in Situ, Hybridization, Stress, Dot Blot, Pituitary). [Doctoral Dissertation]. University of Michigan; 1986. Available from: http://hdl.handle.net/2027.42/127914

13. Adams, Jessica Michelle. A Physiological Role for Hypothalamic Proopiomelanocortin in the Intrinsic Regulation of Locomotor Activity and Stress.

Degree: PhD, Neuroscience, 2015, University of Michigan

URL: http://hdl.handle.net/2027.42/113520

► Proopiomelanocortin (POMC) produced in the hypothalamic arcuate nucleus (Arc) has been studied extensively for its roles in the regulation of food intake and energy expenditure.… (more)

▼ Proopiomelanocortin (POMC) produced in the hypothalamic arcuate nucleus (Arc) has been studied extensively for its roles in the regulation of food intake and energy expenditure. POMC-derived peptides signal satiation and contribute to meal termination, thus individuals lacking POMC exhibit hyperphagic obesity. Neural circuits regulating feeding cross-talk extensively with other neural and endocrine pathways and therefore could affect physiological systems not directly related to feeding. However, these potential functions of ArcPOMC have not been well characterized. We generated a genetic mouse model that lacks Pomc expression specifically in Arc neurons (ArcPomc-knockout (KO)) and used these mice to identify roles for POMC in regulation of locomotor activity and the hypothalamic-pituitary-adrenal (HPA) stress axis. We assessed spontaneous home cage and voluntary wheel running activity in wildtype control mice, obese ArcPomc-KO mice, and ArcPomc-KO mice weight-matched to wildtype controls by caloric restriction. Obese ArcPomc-KO mice had decreased home cage activity that was normalized by weight-matching. In contrast, both obese and weight-matched ArcPomc-KO mice exhibited less voluntary wheel running activity than controls. These results indicate that spontaneous locomotor activity is not directly regulated by ArcPomc but can decrease secondary to obesity. However, ArcPomc intrinsically regulates voluntary wheel running behavior, which is known to be rewarding, independently of body weight, suggesting a reward deficit in ArcPomc-KO mice. Additionally, we extensively characterized the HPA axis of ArcPomc-KO mice. Obese and weight-matched ArcPomc-KO mice developed adrenocortical hypertrophy, and obese ArcPomc-KO mice had elevated stress hormones as well as increased expression of hypothalamic and pituitary HPA axis related genes. We identified hypothalamic arginine vasopressin as a potential downstream effector of this dysregulation, but ArcPomc-KO mice crossed with vasopressin receptor 1b (Avpr1b)-KO mice did not exhibit a rescued HPA phenotype. Therefore, we conclude that ArcPomc tonically inhibits the HPA axis and vasopressin signaling is not necessary for the hyperactivity of the axis caused by POMC-deficiency. Collectively, we have shown that in addition to its role in feeding behavior, ArcPOMC also regulates locomotor activity levels and the HPA stress axis. Both of these pathways are involved in body weight adjustment and may be additional mechanisms whereby POMC deficiency leads to obesity. Advisors/Committee Members: Low, Malcolm J. (committee member), Seasholtz, Audrey (committee member), Olson, David P. (committee member), Becker, Jill B. (committee member), Satin, Leslie (committee member).

Subjects/Keywords: Obesity; Proopiomelanocortin; HPA Stress Axis; Physical Activity; Neurosciences; Health Sciences

…preference for morphine in ArcPomc-KO mice 117 vi Chapter 1: Introduction Proopiomelanocortin… …significance of identified sex differences. 26 Proopiomelanocortin Gene 5’ Exon 1 Exon 2 Exon 3… …3’ Pre-Proopiomelanocortin Precursor Protein Signal Peptide Anterior Pituitary Arcuate… …Nucleus ACTH γ-MSH α-MSH β-LPH CLIP γ-LPH β-Endorphin Figure 1.1: Proopiomelanocortin… …of the neural melanocortin system. LepR: Leptin receptor; POMC: Proopiomelanocortin; AGRP…

10 more images…

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Adams, J. M. (2015). A Physiological Role for Hypothalamic Proopiomelanocortin in the Intrinsic Regulation of Locomotor Activity and Stress. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/113520

Chicago Manual of Style (16^th Edition):

Adams, Jessica Michelle. “A Physiological Role for Hypothalamic Proopiomelanocortin in the Intrinsic Regulation of Locomotor Activity and Stress.” 2015. Doctoral Dissertation, University of Michigan. Accessed April 11, 2021. http://hdl.handle.net/2027.42/113520.

MLA Handbook (7^th Edition):

Adams, Jessica Michelle. “A Physiological Role for Hypothalamic Proopiomelanocortin in the Intrinsic Regulation of Locomotor Activity and Stress.” 2015. Web. 11 Apr 2021.

Vancouver:

Adams JM. A Physiological Role for Hypothalamic Proopiomelanocortin in the Intrinsic Regulation of Locomotor Activity and Stress. [Internet] [Doctoral dissertation]. University of Michigan; 2015. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/2027.42/113520.

Council of Science Editors:

Adams JM. A Physiological Role for Hypothalamic Proopiomelanocortin in the Intrinsic Regulation of Locomotor Activity and Stress. [Doctoral Dissertation]. University of Michigan; 2015. Available from: http://hdl.handle.net/2027.42/113520

14. Madonna, Michael Edward. Melanocotins of the Central Nervous System: Structural Insights on Pigmentation and Appetite.

Degree: Chemistry, 2012, University of California – Santa Cruz

URL: http://www.escholarship.org/uc/item/2sq859qb

► The Melanocortin system of G-Protein coupled receptors and ligands plays a vital role in cell signaling of many important physiological processes, including pigmentation, steroidogenesis, and… (more)

▼ The Melanocortin system of G-Protein coupled receptors and ligands plays a vital role in cell signaling of many important physiological processes, including pigmentation, steroidogenesis, and metabolic control. These receptors are all activated by ligands derived from the proopiomelanocortin (POMC). This prohormone is processed by tissue specific expression of various proteases. Three receptors within this system have a secondary level of regulation. Melanocortin receptors (McRs) 1, 3 and 4 also respond to endogenously expressed antagonist proteins, the agouti-signaling protein (ASIP) and agouti-related protein (AgRP). ASIP and AgRP compete with POMC ligands for receptor binding and signal for reduction in cAMP. Both antagonists are sequentially and structurally similar; yet show differing tissue expression and receptor binding specificities. AgRP is expressed in the hypothalamus and signals for an increase in appetite and lower energy expenditure through Mc3R and Mc4R. ASIP is primarily expressed in the skin and affects pigmentation through Mc1R, but can interact with Mc3R and Mc4R through some genetic mutations. The ligand expression and binding specificity at McRs 1, 3 and 4 provide a unique set of tools for understanding structural determinants required for regulation of pigmentation and energy balance and homeostasis. Here study a novel third antagonist sequence, AgRP2, discovered in teleost fish and expressed in the light sensitive Pineal gland of the brain. This protein shares the same cysteine spacing observed for ASIP and AgRP, and pharmacological studies revealed AgRP2 is selective for the zebrafish Mc1R. Unlike the human homologue, the zebrafish Mc1R is highly expressed in the brain. Knockdown studies reveal that the AgRP2 protein signals for pigment granule aggregation and is a vital molecule in the background adaptive process. Next, NMR analysis of a β-MSH mutant sequence, identified a tyrosine residue, not involved in receptor binding contacts, that participates in forming a turn motif. Mutation of this residue to cysteine significantly reduces this turn structure and dramatically reduces the agonist binding and activity at Mc4R. This mutation predisposes carriers to early-onset obesity. Finally, we study the non-ICK regions of the AgRP protein. Isothermal titration calorimetry experiments implicate the C-loop in proteoglycan binding and motivated rat feeding studies on C-terminal constructs. Through truncation of this domain, a correlation between peptide charge and appetite stimulation was characterized and led to the design of so-called "Super-AgRP" proteins that stimulate feeding in rodents by more than twice that of wild-type AgRP. These studies have the potential to revolutionize the treatment of cachexia and other negative energy balance metabolic disorders.

Subjects/Keywords: Biochemistry; Physical chemistry; Agouti-Related Protein; Melanocortin; Proopiomelanocortin

…proopiomelanocortin (POMC). This prohormone is processed by tissue specific expression of various… …activated by 2 small peptides derived from the proopiomelanocortin (POMC)… …through interactions with agonists derived from proopiomelanocortin (POMC) and the… …ASIP) and 7 Figure 2. Diagram of the proopiomelanocortin (POMC)… …proopiomelanocortin system, Ann N Y Acad Sci 885, 1–21. Seidah, N. G., and Chrétien, M. (1999)…

10 more images…

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Madonna, M. E. (2012). Melanocotins of the Central Nervous System: Structural Insights on Pigmentation and Appetite. (Thesis). University of California – Santa Cruz. Retrieved from http://www.escholarship.org/uc/item/2sq859qb

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):

Madonna, Michael Edward. “Melanocotins of the Central Nervous System: Structural Insights on Pigmentation and Appetite.” 2012. Thesis, University of California – Santa Cruz. Accessed April 11, 2021. http://www.escholarship.org/uc/item/2sq859qb.

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

MLA Handbook (7^th Edition):

Madonna, Michael Edward. “Melanocotins of the Central Nervous System: Structural Insights on Pigmentation and Appetite.” 2012. Web. 11 Apr 2021.

Vancouver:

Madonna ME. Melanocotins of the Central Nervous System: Structural Insights on Pigmentation and Appetite. [Internet] [Thesis]. University of California – Santa Cruz; 2012. [cited 2021 Apr 11]. Available from: http://www.escholarship.org/uc/item/2sq859qb.

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

Council of Science Editors:

Madonna ME. Melanocotins of the Central Nervous System: Structural Insights on Pigmentation and Appetite. [Thesis]. University of California – Santa Cruz; 2012. Available from: http://www.escholarship.org/uc/item/2sq859qb

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

University of Southern California

15. Vargas, Sarah L. Deciphering the neural networks responsible for controlling feeding during and after dehydration-anorexia.

Degree: PhD, Integrative Biology of Disease, 2015, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/559998/rec/1792

► Deciphering the brain circuitry regulating food intake is required to understand metabolic disorders and their co‐morbidities. Energy balance can be tipped in two directions; negatively… (more)

▼ Deciphering the brain circuitry regulating food intake is required to understand metabolic disorders and their co‐morbidities. Energy balance can be tipped in two directions; negatively by forced starvation, or positively by over‐consuming food. Over 30 million people in the US have at some point suffered from an eating disorder (Wade et al., 2011), while 60-80% of advanced cancer patients suffer from cachexia, an end‐stage condition that compromises their desire to eat and often contributes to death (von Haehing et al., 2010). In contrast, approximately 70% of Americans are overweight or obese, predisposing them to diseases such as type II diabetes and cardiovascular disease that can lead to organ failure (Ogden et al., 2012). If such extremes are so destructive, and we are programmed for survival, then which brain networks and mechanisms are disrupted to account for this imbalance? Distinguishing the networks controlling and stimulating food intake are therefore crucial to understanding causation in these important diseases. ❧ The following body of work focuses on identifying the brain networks responsible for compensatory feeding. Compensatory feeding can be described as the motivated feeding that occurs minutes after the reintroduction of normal drinking water, post dehydration. We use the model, Dehydration (DE)‐Anorexia to delineate the network(s) involved. DE‐anorexia occurs when drinking water is replaced with a 2.5% salt solution (HS) for up to 5 days. It causes cellular dehydration, and importantly, reduces food intake and body. When normal drinking water is returned, compensatory feeding is elicited. How these networks are organized and interact to control ingestive behavior of both normal and anorexic states may allow us to overcome dysregulated energy balance and the associated diseases. What makes this a compelling model for some clinical anorexias is that both circulating hormones and neuropeptide expression in DE‐anorexia is commensurate with starvation and should promote feeding; yet similar to clinical anorexias, feeding is strongly inhibited. ❧ Replacing HS with drinking water immediately and profoundly reinstates feeding. Studies from our lab have strongly implicated two hypothalamic regions as contributors to this network: the paraventricular nucleus (PVH) and lateral hypothalamic area (LHA). ❧ The overall aim is to delineate the brain network that drives the compensatory feeding seen when DE‐anorexia is reversed. The following studies focus on investigating the involvement of two networks that converge upon the PVH and LHA to regulate feeding, and is concluded by a set of experiments designed to identify the hindbrain networks activated when DE‐anorexia is reversed and compensatory feeding is stimulated. ❧ In the first two studies found in chapters two and three, we hypothesize that leptin sensitive networks are required for the compensatory feeding seen when DE‐anorexia is reversed. We postulate that reintroducing leptin to these leptin‐ depleted animals would alter ARH NPY and POMC mRNA… Advisors/Committee Members: Watts, Alan G. (Committee Chair), Swanson, Larry W. (Committee Member), Kaslow, Harvey R. (Committee Member), Donovan, Casey D. (Committee Member), Bradley, Nina S. (Committee Member).

Subjects/Keywords: anorexia; dehydration‐anorexia; hypothalamus; neuropeptide‐Y; proopiomelanocortin; feeding; hypertonic saline; paraventricular nucleus; lateral hypothalamic area; nucleus of the solitary tract; glucoprivic feeding; high-fat diet; ventrolateral medulla; leptin

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Vargas, S. L. (2015). Deciphering the neural networks responsible for controlling feeding during and after dehydration-anorexia. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/559998/rec/1792

Chicago Manual of Style (16^th Edition):

Vargas, Sarah L. “Deciphering the neural networks responsible for controlling feeding during and after dehydration-anorexia.” 2015. Doctoral Dissertation, University of Southern California. Accessed April 11, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/559998/rec/1792.

MLA Handbook (7^th Edition):

Vargas, Sarah L. “Deciphering the neural networks responsible for controlling feeding during and after dehydration-anorexia.” 2015. Web. 11 Apr 2021.

Vancouver:

Vargas SL. Deciphering the neural networks responsible for controlling feeding during and after dehydration-anorexia. [Internet] [Doctoral dissertation]. University of Southern California; 2015. [cited 2021 Apr 11]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/559998/rec/1792.

Council of Science Editors:

Vargas SL. Deciphering the neural networks responsible for controlling feeding during and after dehydration-anorexia. [Doctoral Dissertation]. University of Southern California; 2015. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/559998/rec/1792

Freie Universität Berlin

16. Busch, Melanie. Einfluss einer schmerzhaften Entzündung auf die Expression des Proopiomelanocortin-Gens und die β-Endorphin Produktion in Lymphozyten.

Degree: 2007, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-10312

► POMC ist der Precursor verschiedener biologisch aktiver Peptide wie ACTH und END. Neben der Hypophyse produzieren auch nicht-hypophysäre Gewebe wie Immunzellen POMC und die davon… (more)

▼ POMC ist der Precursor verschiedener biologisch aktiver Peptide wie ACTH und END. Neben der Hypophyse produzieren auch nicht-hypophysäre Gewebe wie Immunzellen POMC und die davon abgeleiteten Peptide. Immunzellen setzen END beispielsweise in entzündetem Gewebe frei und durch die Bindung dieses Opioids an Opioidrezeptoren auf peripheren Nervenendigungen kann Entzündungsschmerz vermindert werden. Während alle Sequenzen der biologisch aktiven Peptide auf dem dritten Exon des POMC-Gens kodiert sind, befindet sich die Sequenz zur Translation des Signalpeptids, welches für den Eintritt des Vorläufermoleküls in den sekretorischen Weg unverzichtbar ist, auf dem zweiten Exon. In Lymphozyten wird die Expression von Signalsequenz-kodierender POMC mRNA seit längerem kontrovers diskutiert, da diese Immunzellen vorwiegend am 5`-Ende verkürzte Moleküle ohne Signalsequenz exprimieren. Unter der Annahme, dass die Transkription Signalsequenz-kodierender POMC mRNA unter pathologischen Bedingungen in Lymphozyten induziert wird, untersuchte die vorliegende Studie die Expression von POMC mRNA und den END-Gehalt im drainierenden Lymphknoten im Verlauf einer schmerzhaften, lokalen Pfotenentzündung an Ratten. Mittels RT- und RACE-PCR konnten eine Vielzahl an verschiedenen POMC mRNA-Molekülen identifiziert werden, darunter das schwer detektierbare, Exon 1, 2 und 3 einschließende Full-length POMC und diverse am 5`-Ende verkürzte Moleküle. In Übereinstimmung mit anderen Studien wiesen die verkürzten POMC mRNAs keine Signalsequenz auf. Die Quantifizierung von Exon 2-3 überspannenden POMC mRNA Transkripten mittels qRT-PCR zeigte, dass diese nach 2 Stunden Entzündungszeit um ein Vielfaches hochreguliert wurde, dagegen zeigten sich bei verkürzter POMC mRNA keine Expressionsunterschiede. Da das Expressionsniveau von Exon 2-3 überspannender POMC mRNA nach Induktion der Pfotenentzündung in der Hypophyse unverändert blieb, scheint kein systemischer Effekt an der Erhöhung dieser POMC mRNA in den Lymphozyten beteiligt zu sein. Die Analyse von Lymphknoten mittels Immunfluoreszenz zeigte, dass POMC und END in Lymphknotenzellen co- lokalisiert sind und mittels Durchflusszytometrie und Immunohistochemie konnten Opioidpeptide wie END in T-Helferzellen, in zytotoxischen T-Zellen, in B-Zellen und Monozyten/Makrophagen identifiziert werden. Entsprechend konnte die Expression von Signalsequenz-kodierender POMC mRNA in T- und B-Zellfraktionen separierter Lymphknoten gezeigt werden. T-Lymphozyten exprimierten zudem die mRNA des POMC Prozessierungsenzyms PC2, das für die Konvertierung von beta-LPH in END zuständig ist. In B-Zellen war die Expression von PC2 erst nach Induktion der Entzündung detektierbar. Die Prohormonkonvertase PC1/3, die POMC in ACTH und beta-LPH konvertiert, war ausschließlich in B-Zellen entzündeter Lymphknoten nachweisbar. Die kinetische Peptidanalyse ergab, dass sich der zelluläre END-Gehalt von Lymphozyten innerhalb von 12 - 24 h Entzündungsdauer mehr als verdoppelte. Diese Befunde deuten darauf hin, dass die Neusynthese von END im… Advisors/Committee Members: n (gender), Prof. Dr. med. Michael Schäfer (firstReferee), Prof. Dr. Volker Haucke (furtherReferee).

Subjects/Keywords: Proopiomelanocortin; beta-endorphin; lymphocytes; signal sequence; inflammation; 500 Naturwissenschaften und Mathematik::540 Chemie::540 Chemie und zugeordnete Wissenschaften

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Busch, M. (2007). Einfluss einer schmerzhaften Entzündung auf die Expression des Proopiomelanocortin-Gens und die β-Endorphin Produktion in Lymphozyten. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-10312

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):

Busch, Melanie. “Einfluss einer schmerzhaften Entzündung auf die Expression des Proopiomelanocortin-Gens und die β-Endorphin Produktion in Lymphozyten.” 2007. Thesis, Freie Universität Berlin. Accessed April 11, 2021. http://dx.doi.org/10.17169/refubium-10312.

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

MLA Handbook (7^th Edition):

Busch, Melanie. “Einfluss einer schmerzhaften Entzündung auf die Expression des Proopiomelanocortin-Gens und die β-Endorphin Produktion in Lymphozyten.” 2007. Web. 11 Apr 2021.

Vancouver:

Busch M. Einfluss einer schmerzhaften Entzündung auf die Expression des Proopiomelanocortin-Gens und die β-Endorphin Produktion in Lymphozyten. [Internet] [Thesis]. Freie Universität Berlin; 2007. [cited 2021 Apr 11]. Available from: http://dx.doi.org/10.17169/refubium-10312.

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

Council of Science Editors:

Busch M. Einfluss einer schmerzhaften Entzündung auf die Expression des Proopiomelanocortin-Gens und die β-Endorphin Produktion in Lymphozyten. [Thesis]. Freie Universität Berlin; 2007. Available from: http://dx.doi.org/10.17169/refubium-10312

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

17. Chen, Quinn Kun. Structure-Function Analysis of Endoproteolytic Cleavage: Site-Directed Mutagenesis Studies of the α-MSH Cleavage Site in Silurana tropicalis POMC.

Degree: MS, Biological Sciences, 2009, U of Denver

URL: https://digitalcommons.du.edu/etd/779

► The maturation process of many prohormone molecules typically requires endoproteolytic cleavage C-terminal of dibasic residues, such as the K¹⁴¹R¹⁴²↓ site N-terminal of the α-melanocyte… (more)

Subjects/Keywords: α-MSH; αTC1.9 cells; Endoproteolysis; Fusion protein; Joining peptide; Proopiomelanocortin; Biochemistry, Biophysics, and Structural Biology; Biology; Microbiology

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Chen, Q. K. (2009). Structure-Function Analysis of Endoproteolytic Cleavage: Site-Directed Mutagenesis Studies of the α-MSH Cleavage Site in Silurana tropicalis POMC. (Thesis). U of Denver. Retrieved from https://digitalcommons.du.edu/etd/779

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):

Chen, Quinn Kun. “Structure-Function Analysis of Endoproteolytic Cleavage: Site-Directed Mutagenesis Studies of the α-MSH Cleavage Site in Silurana tropicalis POMC.” 2009. Thesis, U of Denver. Accessed April 11, 2021. https://digitalcommons.du.edu/etd/779.

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

MLA Handbook (7^th Edition):

Chen, Quinn Kun. “Structure-Function Analysis of Endoproteolytic Cleavage: Site-Directed Mutagenesis Studies of the α-MSH Cleavage Site in Silurana tropicalis POMC.” 2009. Web. 11 Apr 2021.

Vancouver:

Chen QK. Structure-Function Analysis of Endoproteolytic Cleavage: Site-Directed Mutagenesis Studies of the α-MSH Cleavage Site in Silurana tropicalis POMC. [Internet] [Thesis]. U of Denver; 2009. [cited 2021 Apr 11]. Available from: https://digitalcommons.du.edu/etd/779.

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

Council of Science Editors:

Chen QK. Structure-Function Analysis of Endoproteolytic Cleavage: Site-Directed Mutagenesis Studies of the α-MSH Cleavage Site in Silurana tropicalis POMC. [Thesis]. U of Denver; 2009. Available from: https://digitalcommons.du.edu/etd/779

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

University of Georgia

18. Johnson, Kenji. Increased TSH producing cells in the pituitary gland of Pax6 haplo-insufficient mice.

Degree: 2016, University of Georgia

URL: http://hdl.handle.net/10724/36188

► Pax6 is a highly conserved transcription factor that is critical for central nervous system development. It is expressed in the eye, forebrain and hindbrain, and… (more)

▼ Pax6 is a highly conserved transcription factor that is critical for central nervous system development. It is expressed in the eye, forebrain and hindbrain, and spinal cord. It is also expressed in the endocrine cells of the pancreas and GI tract, the islets of Langerhans and enteroendocrine cells, respectively. Many of these functions have been reported by studying the effects of a complete absence of Pax6. However, the complete absence of Pax6, in both humans and mice results in the absence of eyes, deformed nasal cavities, and neonate lethality. Pax6 is semidominant such that a mutation in one copy of the gene results in a congenital condition known as Aniridia in humans. Aniridia is defined by the absence of the iris and the ocular phenotypes of this haplo-insufficiency in Pax6 have been well described. However, less is known about how a heterozygous mutation in Pax6 affects other places where Pax6 is expressed. Recently, Aniridic patients have reported an increased propensity for obesity, infertility, polycystic ovarian disease, and severe eczema. Additionally, several lines of evidence suggest an impact on the brain as well as the gut. In this dissertation, we have attempted to illuminate the impact of Pax6 haplo-insufficiency on the endocrine system, including the previously unexplored impact on the pituitary gland and enteroendocrine cells, as well as in the brain. We found that a haplo-insufficiency in Pax6 results in a decrease in GH-producing cells and increase in TSH-producing cells in neonate mice, with the increased TSH-producing cells continuing in adult pituitary glands. This increase in TSH-producing cells results in an increase in circulating levels of T4, although no significant change in circulating T3 levels were found. We also found that a haplo-insufficiency results in structural changes in the adult cerebellum, hippocampus, olfactory bulb, and slight changes in the anterior commissure. Together, these data show that a haplo-insufficiency in Pax6 impacts development and function of a number of organs where Pax6 is expressed and reveals a role for Pax6 in the endocrine system that has previously been unexplored and provides evidence for further studies for the impact of Pax6 haplo-insufficiency.

Subjects/Keywords: Pax6, paired homeobox six; endocrine system; TRH, thyroid releasing hormone; CRH, corticotropin releasing hormone; SST, somatostatin; GHRH, growth hormone releasing hormone; DA, dopamine; GnRH, gonadotropin releasing hormone; POMC, proopiomelanocortin; ACTH, adrenocorticotropin; MSH, melanocortin stimulating hormone, OT, oxytocin; AVP, arganine vasopressin; GH, growth hormone; PRL, prolactin; TSH, thyroid stimulating hormone; LH, leutenizing hormone; FSH, follicle stimulating hormone; T4, thyroxin; T3, triiodothyronine; GLP, glucagon-like peptide; GIP, gastric inhibitory peptide; PC, prohormone convertase; VBM, voxel-based morphometry; MRI, magnetic resonance imaging

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Johnson, K. (2016). Increased TSH producing cells in the pituitary gland of Pax6 haplo-insufficient mice. (Thesis). University of Georgia. Retrieved from http://hdl.handle.net/10724/36188

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):

Johnson, Kenji. “Increased TSH producing cells in the pituitary gland of Pax6 haplo-insufficient mice.” 2016. Thesis, University of Georgia. Accessed April 11, 2021. http://hdl.handle.net/10724/36188.

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

MLA Handbook (7^th Edition):

Johnson, Kenji. “Increased TSH producing cells in the pituitary gland of Pax6 haplo-insufficient mice.” 2016. Web. 11 Apr 2021.

Vancouver:

Johnson K. Increased TSH producing cells in the pituitary gland of Pax6 haplo-insufficient mice. [Internet] [Thesis]. University of Georgia; 2016. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/10724/36188.

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

Council of Science Editors:

Johnson K. Increased TSH producing cells in the pituitary gland of Pax6 haplo-insufficient mice. [Thesis]. University of Georgia; 2016. Available from: http://hdl.handle.net/10724/36188

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

Open Access Theses and Dissertations