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Rutgers University
1.
Al-Baghdadi, Rana Jaber Tarish, 1979-.
Role of activating transcription factor 4 in guiding the liver response to amino acid depletion by asparaginase.
Degree: PhD, Endocrinology and Animal Biosciences, 2016, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/51179/ 
► Asparaginase (ASNase) is widely used to treat acute lymphoblastic leukemia (ALL) in children but it causes metabolic complications related to liver toxicity. ASNase depletes circulating…
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▼ Asparaginase (ASNase) is widely used to treat acute lymphoblastic leukemia (ALL) in children but it causes metabolic complications related to liver toxicity. ASNase depletes circulating asparagine and glutamine, activating the homeostatic amino acid response (AAR) via phosphorylation of eukaryotic initiation factor 2 (eIF2) and resultant synthesis of activating transcription factor 4 (ATF4). The eIF2-ATF4 pathway is essential for cell survival during amino acid starvation conditions. Activation of the AAR in liver requires the eIF2 kinase called general control nonderepressible 2 kinase (GCN2). This pathway is vital to prevent hepatic failure during ASNase treatment. To what extent activation of the GCN2-eIF2-AAR is mediated by ATF4 is unknown. My dissertation objective is to assess the role of ATF4 in directing the hepatic response to ASNase. The overarching hypothesis is that the AAR protects the liver during ASNase treatment. My objective and hypothesis are addressed in three aims: (1) Describe the liver response to ASNase in mice deleted for Atf4; (2) Determine if Atf4 heterozygosity alters the liver response to ASNase; (3) Examine the hepatic response to ASNase in mice with a liver-specific deletion of Atf4. RNA sequencing alongside complementary biochemical and histological approaches were performed in the livers of mice treated with 8 daily injections of ASNase or saline excipient. Cellular pathways examined in detail included the AAR, endoplasmic reticulum (ER) stress response, and the mammalian target of rapamycin complex 1 (mTORC1) signaling pathway. In Aim 1, I discovered that global hepatic gene expression patterns in Atf4 knockout mice overlapped with Gcn2 knockout mice. Shared hepatic pathways or processes altered during ASNase included nuclear receptor activation, mTOR signaling, and xenobiotic metabolism. On the other hand, loss of Atf4 during ASNase uniquely altered gene expression signatures reflecting signaling via eIF2 and ER stress. Further exploration at the level of protein expression and activity in liver revealed that during ASNase Gcn2 deletion stimulated mTORC1 activity whereas Atf4 deletion induced ER stress. In Aim 2, I found that Atf4 heterozygosity compromised the hepatic AAR to ASNase, resulting in greater DNA fragmentation and hepatotoxicity. In Aim 3, I discovered that global hepatic gene expression patterns in nonstressed Atf4 knockout mice reflected many of the same processes and pathways altered in nonstressed mice with a liver-specific deletion of Atf4. Furthermore, the AAR and ER stress profiles in ASNase-treated mice with liver specific deletion of Atf4 were similar in pattern and direction to whole body Atf4 deletion, supporting a role for hepatic ATF4 in directing the adaptive AAR and preventing maladaptive ER stress to ASNase. This research provides insight into the importance of genetic background of patients in choosing ASNase as a treatment. These findings may be used to help predict which patients diagnosed with ALL may be susceptible to adverse metabolic events…
Advisors/Committee Members: Anthony, Tracy G (chair).
Subjects/Keywords: Asparaginase
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APA (6th Edition):
Al-Baghdadi, Rana Jaber Tarish, 1. (2016). Role of activating transcription factor 4 in guiding the liver response to amino acid depletion by asparaginase. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/51179/
Chicago Manual of Style (16th Edition):
Al-Baghdadi, Rana Jaber Tarish, 1979-. “Role of activating transcription factor 4 in guiding the liver response to amino acid depletion by asparaginase.” 2016. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/51179/.
MLA Handbook (7th Edition):
Al-Baghdadi, Rana Jaber Tarish, 1979-. “Role of activating transcription factor 4 in guiding the liver response to amino acid depletion by asparaginase.” 2016. Web. 18 Jan 2021.
Vancouver:
Al-Baghdadi, Rana Jaber Tarish 1. Role of activating transcription factor 4 in guiding the liver response to amino acid depletion by asparaginase. [Internet] [Doctoral dissertation]. Rutgers University; 2016. [cited 2021 Jan 18].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/51179/.
Council of Science Editors:
Al-Baghdadi, Rana Jaber Tarish 1. Role of activating transcription factor 4 in guiding the liver response to amino acid depletion by asparaginase. [Doctoral Dissertation]. Rutgers University; 2016. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/51179/
Rutgers University
2.
Phillipson-Weiner, Lindsey, 1989-.
Role of GCN2 in guiding the cellular and molecular response to asparaginase in the pancreas.
Degree: MS, Nutritional Sciences, 2015, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/48625/
► Asparaginase is a chemotherapy agent used in the treatment of acute lymphoblastic leukemia. Asparaginase can cause severe pancreatitis but the molecular basis is unknown. In…
(more)
▼ Asparaginase is a chemotherapy agent used in the treatment of acute lymphoblastic leukemia. Asparaginase can cause severe pancreatitis but the molecular basis is unknown. In liver of mice, the eIF2 kinase GCN2 is essential for mitigating metabolic stress caused by asparaginase. This study examined the role of GCN2 in the pancreas of mice treated with asparaginase. Eight week old wild type or GCN2 KO mice were injected once daily for 8 d with either 3 IU/
g BW of saline or asparaginase. Eight hours after final injection, mice were sacrificed and pancreata were weighed and harvested. In GCN2 KO mice treated with asparaginase, pancreas weights were significantly increased (P<0.05) and the organs visibly enlarged. Histological examination revealed ductal dilatation and swollen acinar cells in GCN2 KO only. Oil red O staining and measurement of pancreas triglycerides ruled out lipid accumulation as a contributing factor. No signs of cell death by TUNEL stain were detected in the pancreas, and serum amylase activity did not differ among treatment groups. However, Pancreatitis Associated Protein (PAP) mRNA expression was elevated in livers of asparaginase-treated GCN2 KO mice only. Phosphorylation of eIF2 and pancreatic expression of asparagine synthetase were similar among treatment groups, but mTORC1 signaling was decreased to the greatest extent in the pancreata of asparaginase-treated GCN2 KO mice. Additionally, transmission electron microscopy revealed evidence of ER stress in GCN2 KO mice treated with asparaginase. These data suggest that loss of GCN2 predisposes the pancreas toward the development of asparaginase-associated pancreatitis. NIH HD070487
Advisors/Committee Members: Anthony, Tracy G (chair), Watford, Malcolm (internal member), McAuliffe, Geoffrey (outside member).
Subjects/Keywords: Asparaginase; Pancreatitis
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APA (6th Edition):
Phillipson-Weiner, Lindsey, 1. (2015). Role of GCN2 in guiding the cellular and molecular response to asparaginase in the pancreas. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/48625/
Chicago Manual of Style (16th Edition):
Phillipson-Weiner, Lindsey, 1989-. “Role of GCN2 in guiding the cellular and molecular response to asparaginase in the pancreas.” 2015. Masters Thesis, Rutgers University. Accessed January 18, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/48625/.
MLA Handbook (7th Edition):
Phillipson-Weiner, Lindsey, 1989-. “Role of GCN2 in guiding the cellular and molecular response to asparaginase in the pancreas.” 2015. Web. 18 Jan 2021.
Vancouver:
Phillipson-Weiner, Lindsey 1. Role of GCN2 in guiding the cellular and molecular response to asparaginase in the pancreas. [Internet] [Masters thesis]. Rutgers University; 2015. [cited 2021 Jan 18].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/48625/.
Council of Science Editors:
Phillipson-Weiner, Lindsey 1. Role of GCN2 in guiding the cellular and molecular response to asparaginase in the pancreas. [Masters Thesis]. Rutgers University; 2015. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/48625/
Rutgers University
3.
Hassanien, Sarah, 1989-.
Characterization of the novel h82r mutation in cgi-58 that causes neutral lipid storage disorder in humans.
Degree: MS, Nutritional Sciences, 2014, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/45289/
► Comparative gene identification-58 (CGI-58) interacts with and co-activates adipose triglyceride lipase (ATGL). The H82R mutation in human CGI-58 causes a neutral lipid storage disorder (NLSD)…
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▼ Comparative gene identification-58 (CGI-58) interacts with and co-activates adipose triglyceride lipase (ATGL). The H82R mutation in human CGI-58 causes a neutral lipid storage disorder (NLSD) characterized by ichthyosis and excessive triacylglycerol storage in many types of cells. We studied the comparable H84R mutation in mouse CGI-58, and H84A mutated CGI-58, to ask how CGI-58 function is impaired. The ectopic expression of wild-type (WT) CGI-58 in human NLSD fibroblasts reduced excessive triglyceride storage to normal levels, whereas H84R CGI-58 was ineffective. Additionally, H84R CGI-58 failed to co-activate ATGL in an in vitro triglyceride hydrolase assay and H84A CGI-58 was not as efficient, when compared to WT CGI-58. Immunofluorescence microscopy revealed that H84R and H84A CGI-58 localized to ectopic perilipin 1A on lipid droplets of cultured NIH3T3CARΔ fibroblasts as well as WT CGI-58. Moreover, the addition of forskolin and isobutylmethylxanthine to the cells triggered the dispersion of all three variants of CGI-58 from the perilipin scaffold into the cytoplasm. A co-immunoprecipitation assay demonstrated that H84R and H84A CGI-58 bound ATGL as well as WT CGI-58. Additionally, while WT CGI-58 and ATGL can be individually recruited to lipid droplets and ATGL recruitment to lipid droplets is increased in the presence of CGI-58, the H84R and H82R mutations do not interfere with lipid droplet recruitment of CGI-58 with ATGL. Thus, although H84R CGI-58 shows appropriate subcellular localization in cells expressing perilipin 1A, binds to ATGL, and is effectively recruited to lipid droplets, it does not co-activate ATGL’s hydrolase activity. Future experiments are needed to explore additional mechanisms for deficient function of H84R CGI-58.
Advisors/Committee Members: Brasaemle, Dawn L. (chair), Storch, Judith (internal member), Anthony, Tracy G. (internal member).
Subjects/Keywords: Lipids – Metabolism – Disorders
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APA (6th Edition):
Hassanien, Sarah, 1. (2014). Characterization of the novel h82r mutation in cgi-58 that causes neutral lipid storage disorder in humans. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/45289/
Chicago Manual of Style (16th Edition):
Hassanien, Sarah, 1989-. “Characterization of the novel h82r mutation in cgi-58 that causes neutral lipid storage disorder in humans.” 2014. Masters Thesis, Rutgers University. Accessed January 18, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/45289/.
MLA Handbook (7th Edition):
Hassanien, Sarah, 1989-. “Characterization of the novel h82r mutation in cgi-58 that causes neutral lipid storage disorder in humans.” 2014. Web. 18 Jan 2021.
Vancouver:
Hassanien, Sarah 1. Characterization of the novel h82r mutation in cgi-58 that causes neutral lipid storage disorder in humans. [Internet] [Masters thesis]. Rutgers University; 2014. [cited 2021 Jan 18].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/45289/.
Council of Science Editors:
Hassanien, Sarah 1. Characterization of the novel h82r mutation in cgi-58 that causes neutral lipid storage disorder in humans. [Masters Thesis]. Rutgers University; 2014. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/45289/
Rutgers University
4.
Al-Yasari, Ali Mosa Rashid, 1981-.
Does preconception alcohol abuse make the offspring vulnerable to developing type II diabetes?.
Degree: PhD, Endocrinology and Animal Biosciences, 2017, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/55304/
► Recently, it was reported in our laboratory that binge-like alcohol drinking for three weeks prior to conception by female rats produces poor birth outcome and…
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▼ Recently, it was reported in our laboratory that binge-like alcohol drinking for three weeks prior to conception by female rats produces poor birth outcome and defects in the offspring’s body stress response. These effects occur even after alcohol abstinence prior to conception, during pregnancy and postnatal care. Offspring born after preconception alcohol exposures (PCAE) show abnormalities in expression of the stress regulatory gene Pro-opiomelanocortin (Pomc) in the hypothalamus, resulting in higher stress hormone responses to a stress challenge and increased anxiety-like behavior. Since stress is often connected with increased body risk for metabolic diseases and since POMC-expressing neurons are known to control glucose homeostasis, I hypothesized that PCAE disrupts POMC neuronal function to increase susceptibility to developing hyperglycemia in animals. To test this hypothesis, I determined if PCAE had the ability to alter glucose homeostasis and increase the susceptibility to develop high fat diet (HFD)-streptozotocin (STZ)-induced diabetes in the offspring. The aims of my study were to determine the effects of PCAE on pancreatic, hepatic, and hypothalamic POMC/BEP neuronal abnormalities, and how the BEP replacement ameliorates these effects. In this study, 21 female adult Sprague Dawley rats were divided body weight-matched and randomly into three groups; the control group receiving rat chow and water ad libitum (AD; N=7), the alcohol-fed group (AF; N=7) receiving a liquid diet containing ethanol (6.7%), or the calorie-matched pair-fed (PF; N=7) group receiving an isocaloric liquid control diet. After 30 days of feeding, all rats were given normal chow ad libitum for three weeks; the estrus cycle was monitored and bred them with normal adult males to produce offspring. The pups were weaned at the age of postnatal day (PND) 25 and were randomly selected one animal from each litter to have three body weight-matched different groups (AD, PF, and AF, N=7). At the age of two months, offspring of AF exposed animals showed significantly higher fasting blood glucose and leptin and lower insulin and glucagon levels as compared with AD and PF offspring. Oral glucose tolerance test (OGTT) and intraperitoneal insulin tolerance test (IPITT) data showed higher blood glucose and lower insulin production in AF in comparison with AD and PF offspring. Further, glucose-stimulated insulin secretion (GSIS) results demonstrated that AF group showed lowest insulin secretion as a response to an oral glucose solution in comparison with AD and PF groups. To evaluate the mechanistic link between PCAE effects on pancreatic homeostasis, I measured inflammatory markers such as; COX-2, IFN-γ, IL-6, and CD3 in whole (endocrine & exocrine) pancreatic tissue, insulin and glucagon in pancreatic islets by immunohistochemistry (IHC). Compared to AD and PF control groups, offspring from AF animals displayed higher levels of inflammatory markers accompanied with low pancreatic insulin and high glucagon expression, indicating the metabolic…
Advisors/Committee Members: Sarkar, Dipak K (chair), Bello, Nicholas T (internal member), Anthony, Tracy G (internal member), Haimovich, Beatrice (outside member), School of Graduate Studies.
Subjects/Keywords: Diabetes; Alcoholism
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APA (6th Edition):
Al-Yasari, Ali Mosa Rashid, 1. (2017). Does preconception alcohol abuse make the offspring vulnerable to developing type II diabetes?. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/55304/
Chicago Manual of Style (16th Edition):
Al-Yasari, Ali Mosa Rashid, 1981-. “Does preconception alcohol abuse make the offspring vulnerable to developing type II diabetes?.” 2017. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/55304/.
MLA Handbook (7th Edition):
Al-Yasari, Ali Mosa Rashid, 1981-. “Does preconception alcohol abuse make the offspring vulnerable to developing type II diabetes?.” 2017. Web. 18 Jan 2021.
Vancouver:
Al-Yasari, Ali Mosa Rashid 1. Does preconception alcohol abuse make the offspring vulnerable to developing type II diabetes?. [Internet] [Doctoral dissertation]. Rutgers University; 2017. [cited 2021 Jan 18].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/55304/.
Council of Science Editors:
Al-Yasari, Ali Mosa Rashid 1. Does preconception alcohol abuse make the offspring vulnerable to developing type II diabetes?. [Doctoral Dissertation]. Rutgers University; 2017. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/55304/
Rutgers University
5.
Margolies, Nicholas.
Role of ATF4 in dietary sulfur amino acid restriction.
Degree: MS, Endocrinology and Animal Biosciences, 2018, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/59164/
► Dietary sulfur amino acid restriction (SAAR) increases food intake and energy expenditure and improves body composition. Dietary SAAR activates the integrated stress response (ISR), which…
(more)
▼ Dietary sulfur amino acid restriction (SAAR) increases food intake and energy expenditure and improves body composition. Dietary SAAR activates the integrated stress response (ISR), which orchestrates transcriptional changes through activating transcription factor 4 (ATF4). Fibroblast growth factor 21 (FGF21) is a hepatokine and ATF4 target which affects food and fluid intake, energy expenditure, and body composition. To determine whether ATF4 is needed to increase food and fluid intake and energy expenditure, improve body composition, and alter hepatic gene expression during SAAR, male and female wild type (WT) and Atf4-/- (KO) mice were maintained on a high fat (60% fat by Kcal) control (0.86% Met, 0% Cys) or high fat SAAR (0.12% Met, 0% Cys) diet for 5 weeks. SAAR increased hepatic Fgf21 and water intake independently of ATF4 in males and females. In males, SAAR increased food intake and energy expenditure independently of ATF4, while females showed no response. SAAR improved body composition in WT males but not females and did not prevent increased adiposity in male KO mice. ATF4 is required for protection from adiposity but not for increased food and water intake, energy expenditure, or hepatic Fgf21 expression during SAAR. FGF21 does not work exclusively through an ATF4-FGF21 axis and may be driving ATF4-independent responses to SAAR.
Advisors/Committee Members: Anthony, Tracy G (chair), Bello, Nicholas T (internal member), Belden, William (internal member), School of Graduate Studies.
Subjects/Keywords: Dietary sulfur amino acid restriction; ATF4
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APA (6th Edition):
Margolies, N. (2018). Role of ATF4 in dietary sulfur amino acid restriction. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/59164/
Chicago Manual of Style (16th Edition):
Margolies, Nicholas. “Role of ATF4 in dietary sulfur amino acid restriction.” 2018. Masters Thesis, Rutgers University. Accessed January 18, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/59164/.
MLA Handbook (7th Edition):
Margolies, Nicholas. “Role of ATF4 in dietary sulfur amino acid restriction.” 2018. Web. 18 Jan 2021.
Vancouver:
Margolies N. Role of ATF4 in dietary sulfur amino acid restriction. [Internet] [Masters thesis]. Rutgers University; 2018. [cited 2021 Jan 18].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/59164/.
Council of Science Editors:
Margolies N. Role of ATF4 in dietary sulfur amino acid restriction. [Masters Thesis]. Rutgers University; 2018. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/59164/
Rutgers University
6.
Pinkerton, Mark Hurst.
Reconstitution of processive selenocysteine incorporation in wheat germ lysate provides insight into selenocysteine insertion sequence binding proteins.
Degree: PhD, Biomedical Sciences, 2019, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/61908/
► A UGA stop codon is recoded to accommodate the incorporation of the 21st amino acid selenocysteine (Sec). For a UGA to be recoded a specialized…
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▼ A UGA stop codon is recoded to accommodate the incorporation of the 21st amino acid selenocysteine (Sec). For a UGA to be recoded a specialized set of cis and trans factors are required and consist of: an mRNA with an in frame UGA codon, a selenocysteine insertion sequence (SECIS) in the 3’ untranslated region (3’ UTR), a SECIS binding protein 2 (SBP2), a specific translation elongation factor (eEFSec), and a selenocysteine tRNA (Sec-tRNA[Ser]Sec). The N-terminus of SBP2 is believed to have no direct role in Sec incorporation because the C terminus of SBP2 is sufficient for the incorporation of Sec into selenoproteins that have one Sec codon. Selenoprotein P (SELENOP) is an essential selenoprotein for male fertility and proper neuron function. SELENOP is also unique in that it contains 10 selenocysteines and is involved in selenium uptake and transport. Interestingly, an in vitro translation system using wheat germ lysate, has no endogenous selenocysteine incorporation factors, cannot synthesize full length SELENOP even when all the known factors are added. The aim of this thesis is to gain insight into the mechanism of processive eukaryotic selenocysteine incorporation by in vitro reconstitution and bioinformatics.
Advisors/Committee Members: Brewer, Gary (chair), Copeland, Paul R (internal member), Madura, Kiran (internal member), Anthony, Tracy G (outside member), School of Graduate Studies.
Subjects/Keywords: Translation; Selenoproteins
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APA (6th Edition):
Pinkerton, M. H. (2019). Reconstitution of processive selenocysteine incorporation in wheat germ lysate provides insight into selenocysteine insertion sequence binding proteins. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/61908/
Chicago Manual of Style (16th Edition):
Pinkerton, Mark Hurst. “Reconstitution of processive selenocysteine incorporation in wheat germ lysate provides insight into selenocysteine insertion sequence binding proteins.” 2019. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/61908/.
MLA Handbook (7th Edition):
Pinkerton, Mark Hurst. “Reconstitution of processive selenocysteine incorporation in wheat germ lysate provides insight into selenocysteine insertion sequence binding proteins.” 2019. Web. 18 Jan 2021.
Vancouver:
Pinkerton MH. Reconstitution of processive selenocysteine incorporation in wheat germ lysate provides insight into selenocysteine insertion sequence binding proteins. [Internet] [Doctoral dissertation]. Rutgers University; 2019. [cited 2021 Jan 18].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/61908/.
Council of Science Editors:
Pinkerton MH. Reconstitution of processive selenocysteine incorporation in wheat germ lysate provides insight into selenocysteine insertion sequence binding proteins. [Doctoral Dissertation]. Rutgers University; 2019. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/61908/
Rutgers University
7.
Zhu, Qiaoqiao, 1991-.
Crosstalk between long non-coding RNAs and circadian chromatin.
Degree: PhD, Circadian rhythms, 2020, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/64311/
► The circadian rhythm is governed by transcriptional negative feedback facilitated by oscillating histone modifications and chromatin remodeling. The circadian rhythm is entrained by external zeitgebers…
(more)
▼ The circadian rhythm is governed by transcriptional negative feedback facilitated by oscillating histone modifications and chromatin remodeling. The circadian rhythm is entrained by external zeitgebers (light and temperature) and are conserved in Neurospora, Drosophila, zebrafish, and mammals. The clock gene frequency in Neurospora and Period2 in vertebrates have natural antisense transcripts (NATs) whose function is not understood. In this dissertation I examined the connection among the circadian clock, non-coding RNAs and heterochromatin formation on both on the genome-wide and locus-specific level using a multi-organism approach. I performed a genome-wide study, using RNA-seq and ChIP-seq to understand the role of H3 lysine 4 methyltransferase (KMT2/SET-1) and histone H3 lysine 9 methyltransferase (KMT1/DIM-5) in Neurospora to understand the role of 2 seemingly opposing modifications. Integrated analysis of RNA-seq and ChIP-seq showed crosstalk and redistributions between histone H3 lysine 4 tri-methylation (H3K4me3) and histone H3 lysine 9 tri-methylation (H3K9me3). I also examined how perturbing the expression of a diurnal lncRNA affected downstream heterochromatin formation at the telomeres. The core circadian clock controls rhythms in TERRA, a long noncoding RNA that originates from telomeres and my research shows alcohol disrupts the diurnal rhythm in TERRA and heterochromatin at the telomere, which in theory makes telomeres more susceptible to DNA damage. I also examined the Per2 NAT, Per2AS and found the diurnal rhythm in Per2AS is dependent on BMAL1. Using the ChIRP-MS, I identified Per2AS-interacting proteins. Specifically, I found hnRNP M interacts with Per2AS and hnRNP M is required to maintain the normal amplitude and period of Per2. Furthermore, I demonstrate that hnRNP M is necessary for H3K9me3 and H3K27me3 at Per2. These findings support a model where Per2AS may serve as scaffold for hnRNP M and other associated proteins that assist in heterochromatin formation at Per2. Collectively, this dissertation furthers our understanding of the circadian clock, non-coding RNAs, and circadian regulated facultative heterochromatin formation.
Advisors/Committee Members: Belden, William J. (chair), Anthony, Tracy G (internal member), Sarkar, Dipak (internal member), Lee, KiBum (outside member), School of Graduate Studies.
Subjects/Keywords: Ribonucleases; Endocrinology and Animal Biosciences
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APA (6th Edition):
Zhu, Qiaoqiao, 1. (2020). Crosstalk between long non-coding RNAs and circadian chromatin. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/64311/
Chicago Manual of Style (16th Edition):
Zhu, Qiaoqiao, 1991-. “Crosstalk between long non-coding RNAs and circadian chromatin.” 2020. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/64311/.
MLA Handbook (7th Edition):
Zhu, Qiaoqiao, 1991-. “Crosstalk between long non-coding RNAs and circadian chromatin.” 2020. Web. 18 Jan 2021.
Vancouver:
Zhu, Qiaoqiao 1. Crosstalk between long non-coding RNAs and circadian chromatin. [Internet] [Doctoral dissertation]. Rutgers University; 2020. [cited 2021 Jan 18].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/64311/.
Council of Science Editors:
Zhu, Qiaoqiao 1. Crosstalk between long non-coding RNAs and circadian chromatin. [Doctoral Dissertation]. Rutgers University; 2020. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/64311/
Rutgers University
8.
Tuazon, Marc A.
Hepatic triglyceride metabolism in response to acute and chronic exercise: a tale of two intensities.
Degree: PhD, Nutritional Sciences, 2015, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/47597/
► Impaired hepatic triglyceride (TG) metabolism is associated with dysfunctions such as insulin resistance and elevated VLDL-TG secretion. Chronic exercise lowers plasma TG and hepatic TG,…
(more)
▼ Impaired hepatic triglyceride (TG) metabolism is associated with dysfunctions such as insulin resistance and elevated VLDL-TG secretion. Chronic exercise lowers plasma TG and hepatic TG, however, many benefits of chronic exercise are due to repeated effects of single exercise sessions. Little is known, however, about effects of acute exercise on hepatic TG metabolism or the influence of exercise intensity in males vs. females. We examined impacts of single bouts of moderate-intensity continuous exercise (CE) vs. high-intensity interval exercise (HIIE) on hepatic TG metabolism and secretion in mice of both sexes. Hepatic TG was transiently increased on the day of exercise and in females the increase was greater with HIIE. These exercise-related changes appeared driven by enhanced transcription of the lipid-droplet coating protein Perilipin 2. On the day after exercise, VLDL-TG secretion rate was only reduced by HIIE in females. These findings demonstrated intensity-dependent and sex-specific effects of acute exercise. Because of our findings that single bouts of HIIE alter hepatic TG metabolism more than CE and the potential for chronic exercise to attenuate severity of complications associated with menopause, we compared 6 weeks of training using these exercise types on hepatic TG metabolism and secretion, glucose tolerance, body composition, and strength in ovariectomized (OVX) and sham-operated (SHAM) mice. Additionally, we measured energy expenditure and substrate oxidation during and immediately after exercise and assessed post-exercise spontaneous physical activity (SPA) to further characterize these exercise modalities. In OVX and SHAM, CE and HIIE elicited similar energy expenditures during exercise and in the post-exercise period lowered absolute carbohydrate oxidation and SPA. OVX vs. SHAM displayed impaired glucose tolerance, elevated blood glucose, and greater body fat despite lower hepatic TG, as well as lower strength, and these outcomes were not affected by training. In contrast to responses to single exercise sessions, chronic HIIE increased hepatic AMPK protein. Further, the reduction in VLDL-TG secretion after a single HIIE session was not maintained after training. These results reveal intensity-dependent effects of habitual exercise on hepatic AMPK expression and with our findings of single bouts reveal distinct responses in hepatic TG metabolism to acute vs. chronic exercise.
Advisors/Committee Members: Campbell, Sara C (chair), Anthony, Tracy G (internal member), Arent, Shawn M (internal member), Brasaemle, Dawn L (internal member), McKeever, Kenneth H (outside member).
Subjects/Keywords: Triglycerides – Metabolism; Exercise
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APA (6th Edition):
Tuazon, M. A. (2015). Hepatic triglyceride metabolism in response to acute and chronic exercise: a tale of two intensities. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/47597/
Chicago Manual of Style (16th Edition):
Tuazon, Marc A. “Hepatic triglyceride metabolism in response to acute and chronic exercise: a tale of two intensities.” 2015. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/47597/.
MLA Handbook (7th Edition):
Tuazon, Marc A. “Hepatic triglyceride metabolism in response to acute and chronic exercise: a tale of two intensities.” 2015. Web. 18 Jan 2021.
Vancouver:
Tuazon MA. Hepatic triglyceride metabolism in response to acute and chronic exercise: a tale of two intensities. [Internet] [Doctoral dissertation]. Rutgers University; 2015. [cited 2021 Jan 18].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/47597/.
Council of Science Editors:
Tuazon MA. Hepatic triglyceride metabolism in response to acute and chronic exercise: a tale of two intensities. [Doctoral Dissertation]. Rutgers University; 2015. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/47597/
Rutgers University
9.
Klein, Dylan Joseph, 1990-.
Fit as a horse: from skeletal muscle metabolism to whole-body physiology.
Degree: PhD, Nutritional Sciences, 2018, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/59137/
► There is little information regarding the molecular events that govern the beneficial adaptations of equine skeletal muscle in response to acute exercise and training. This…
(more)
▼ There is little information regarding the molecular events that govern the beneficial adaptations of equine skeletal muscle in response to acute exercise and training. This work addressed this subject in two manners. First, based on the comparative mammalian literature, signaling and gene expression markers related to S-ER stress and proteostasis were analyzed in equine gluteus medius biopsies before and after acute high-intensity exercise in the untrained and trained states. Protein expression analysis revealed that S-ER stress signaling was apparent, however, many downstream mRNA expression markers were not significantly impacted by acute high-intensity fatiguing exercise in the untrained state. Twelve wks of training, however, altered S-ER stress signaling as well as the expression of genes related to apoptosis and protein degradation. Additionally, mRNA expression markers of protein degradation were not impacted by acute fatiguing exercise in the untrained state; however, training status did alter the exercise-induced gene expression of the E3-ubiquitin ligase, Fbxo32. Lastly, training also compressed the mRNA expression variability in most S-ER stress-related genes, both basally and post-exercise.
Second, based on the gene expression data, a non-targeted metabolomics approach was employed in order to assess the phenotypic variability in skeletal muscle at the level of metabolites. Metabolic differences in the early (3 h) and late (24 h) recovery periods were also assessed. In agreement with the gene expression findings, PCA and hierarchical clustering analysis of muscle biopsies revealed that training dominated the skeletal muscle phenotype and produced a homogeneous basal and exercise-induced metabolic signature among the horses. Early metabolic alterations largely centered on the branched-chain amino acids, microbial-derived xenobiotics, and a variety of lipid and nucleotide-derived compounds, especially in the trained state. Further, training increased the abundances of almost every identified long-chain free-fatty acid and complex lipid species in the pre-exercise condition. These elevations declined over 24 h following acute fatiguing exercise and were associated with increased gene expression related to lipid uptake and utilization.
Finally, in an extension of the first two studies, the final objective of this work was to identify the impacts of prolonged training and detraining on body composition and aerobic and athletic capacities, as very little information exists regarding these training periods in the horse. Twelve wks of training caused a robust increase in VO2max and athletic capacity, with geldings outperforming mares. There was, however, no concomitant improvement in body composition during this period. An additional 60 wks of training was accompanied by a worsening of body composition in both sexes whereas aerobic capacity and athletic capabilities were maintained. Interestingly, 20 wks of detraining resulted in a maintenance of VO2max and performance despite a statistically significant…
Advisors/Committee Members: Anthony, Tracy G (chair), McKeever, Kenneth H (co-chair), Watford, Malcolm (internal member), Shapses, Sue (internal member), Arent, Shawn (internal member), Malinowski, Karyn (outside member), School of Graduate Studies.
Subjects/Keywords: Horses – Physiology; Horses – Exercise; Horses – Genetics
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APA (6th Edition):
Klein, Dylan Joseph, 1. (2018). Fit as a horse: from skeletal muscle metabolism to whole-body physiology. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/59137/
Chicago Manual of Style (16th Edition):
Klein, Dylan Joseph, 1990-. “Fit as a horse: from skeletal muscle metabolism to whole-body physiology.” 2018. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/59137/.
MLA Handbook (7th Edition):
Klein, Dylan Joseph, 1990-. “Fit as a horse: from skeletal muscle metabolism to whole-body physiology.” 2018. Web. 18 Jan 2021.
Vancouver:
Klein, Dylan Joseph 1. Fit as a horse: from skeletal muscle metabolism to whole-body physiology. [Internet] [Doctoral dissertation]. Rutgers University; 2018. [cited 2021 Jan 18].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/59137/.
Council of Science Editors:
Klein, Dylan Joseph 1. Fit as a horse: from skeletal muscle metabolism to whole-body physiology. [Doctoral Dissertation]. Rutgers University; 2018. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/59137/
10.
Kochem, Matthew C.
Sweeteners, sweet antagonists, and metabolism.
Degree: PhD, Nutritional Sciences, 2017, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/52214/
► Sugars and sweeteners are proposed to stimulate human sweet taste via the receptor, T1R2-T1R3. T1R2-T1R3 is a heterodimeric GPCR expressed in oral taste tissue. T1R2-T1R3…
(more)
▼ Sugars and sweeteners are proposed to stimulate human sweet taste via the receptor, T1R2-T1R3. T1R2-T1R3 is a heterodimeric GPCR expressed in oral taste tissue. T1R2-T1R3 binds sugars, non-nutritive sweeteners, and sweet taste blockers. It was recently discovered that T1R2-T1R3 is also expressed in extra-oral tissues including the intestine, hypothalamus, pancreas, and adipose. This finding is striking because non-nutritive sweeteners are believed to be metabolically inert. Hence, it raises the question of whether T1R2-T1R3 plays a role not only sweet taste perception but also in regulatory and metabolic physiology. The purpose of this research project is to investigate the perceptual and physiological functions of T1R2-T1R3 using a pharmacological approach in human participants. In the first aim, I determined whether glucose and fructose behave as partial agonists of the sweet taste receptor and can enhance or suppress each other in mixture. In the second aim, I sought to assess and improve the sweetness of glucose and its metabolic profile relative to fructose and sucrose. In the third aim, I conducted psychophysical studies to determine whether metabolically active drugs act on the sweet taste receptor. In the fourth aim, I conducted glucose tolerance studies to determine whether sweet taste stimuli influence glucose metabolism. And in the fifth aim, I conducted glucose tolerance tests to determine whether sweet taste inhibitors influence glucose metabolism. I found that sweeteners and antagonists had both perceptual and physiological functions. In the first aim, I demonstrated that glucose is a poor sweetener relative to fructose because it is not a full agonist of the sweet receptor. In the second aim, I demonstrated that glucose can be rendered almost indistinguishable from sucrose at the same caloric level with the addition of a non-nutritive sweetener. Thus, the difference in glucose and fructose sweetness can be overcome when adding stevioside to glucose. In the third aim, I demonstrated that clofibric acid, a lipid lowering prescription drug, inhibits sweet taste perception. Since it has been shown to inhibit T1R3 in vitro, I conclude from our data that it is also a T1R3 inhibitor in vivo. In the fourth aim, I demonstrated that high potency sweeteners (HPS), which are thought to be metabolically inert, enhance insulin and glucose responses relative to a standard OGTT. And in the fifth aim, I found that sweet taste blockers caused an opposite reaction and slowed glucose rise in the blood relative to a standard OGTT. As a sugar receptor, T1R2-T1R3 imparts a powerful influence on human health by guiding food choice and metabolism. My findings are of public health relevance because excessive intake of sweet tasting compounds such as sugars and other sweeteners are a major long-term health concern. Overconsumption of dietary sugars, particularly in the form of sweetened beverages, is thought to promote obesity, diabetes, fatty liver disease, and metabolic syndrome. Despite efforts to curb…
Advisors/Committee Members: Breslin, Paul A (chair), Anthony, Tracy G (internal member), Miller, Joshua W (internal member), Margolskee, Robert F (outside member).
Subjects/Keywords: Nutrition; Sweeteners
…recruited from the Rutgers University New Brunswick campus. Subjects were
paid to participate and…
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APA ·
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APA (6th Edition):
Kochem, M. C. (2017). Sweeteners, sweet antagonists, and metabolism. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/52214/
Chicago Manual of Style (16th Edition):
Kochem, Matthew C. “Sweeteners, sweet antagonists, and metabolism.” 2017. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/52214/.
MLA Handbook (7th Edition):
Kochem, Matthew C. “Sweeteners, sweet antagonists, and metabolism.” 2017. Web. 18 Jan 2021.
Vancouver:
Kochem MC. Sweeteners, sweet antagonists, and metabolism. [Internet] [Doctoral dissertation]. Rutgers University; 2017. [cited 2021 Jan 18].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/52214/.
Council of Science Editors:
Kochem MC. Sweeteners, sweet antagonists, and metabolism. [Doctoral Dissertation]. Rutgers University; 2017. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/52214/
11.
Xu, Heli, 1991-.
Fat and fit: metabolic changes in skeletal muscle of liver fatty acid-binding protein knockout mice.
Degree: PhD, Fatty acids, 2019, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/61041/
► Liver fatty acid-binding protein (LFABP, FABP1) is abundantly expressed in the liver and small intestine, and thought to facilitate hepatic and intestinal lipid trafficking into…
(more)
▼ Liver fatty acid-binding protein (LFABP, FABP1) is abundantly expressed in the liver and small intestine, and thought to facilitate hepatic and intestinal lipid trafficking into various metabolic pathways with its high binding affinity for long chain fatty acids. Moreover, LFABP has also been implicated in regulating systemic energy homeostasis based on studies of LFABP null (LFABP-/-) mice. We and others have previously reported that LFABP-/- mice exhibit greater body weight gain and body fat mass in response to high fat feeding compared with wild-type (WT) mice. Despite being more obese, however, LFABP-/- mice were protected from high fat feeding-induced decline in exercise capacity, showing an approximate doubling of running distance compared with WT mice on the high fat diet. In studies aimed at understanding the metabolic changes in skeletal muscle underlying this surprising exercise phenotype in LFABP-/- mice, we found significantly higher triglyceride and glycogen content, as well as increased mitochondrial enzyme activities and fatty acid oxidation capacity in the resting muscles of LFABP-/- mice, suggesting a greater substrate storage and mitochondrial function at resting state. During a low intensity exercise, LFABP-/- mice showed a preference for carbohydrate utilization in the first 10 min of the exercise and switched to a higher lipid utilization compared with WT during the rest 10 min of exercise, with greater exercise-dependent decreases in muscle glycogen stores and elevated free fatty acid in the plasma after exercise. Using cellular bioenergetics measurements, primary myoblasts from high fat-fed LFABP-/- mice showed a higher respiratory capacity compared with WT mice, supporting the increased exercise capacity of LFABP-/- mice. Interestingly, primary myotubes from chow-fed mice treated with fatty acids only showed modest difference between the genotypes, suggesting that apart from a high concentration of plasma FAs, other circulating mediators may be required for the improved muscle energy metabolism in high fat fed-LFABP-/- mice. In examining potential interorgan signaling possibilities, we found similar insulin sensitivity in skeletal muscle between the genotypes, suggesting an insulin-independent mechanism mediating the muscle metabolic changes in LFABP-/- mice. Moreover, we found decreased FGF21 expression levels in the liver and trending lower FGF21 levels in the plasma of LFABP-/- mice, despite our previous report that LFABP-/- mice showed trending higher plasma levels of adiponectin, a downstream target of FGF21. However, we found similar FGF21 sensitivity in epidydimal adipose tissues between the genotypes and trending lower expression levels of adiponectin in the epidydimal adipose tissues, suggesting that FGF21-meidated adiponectin production and secretion may be enhanced in other fat depots. Overall, muscle metabolic reprogramming in LFABP-/- mice underlies their resistance to high fat feeding-induced decline in exercise capacity, including increased substrate availability and improved…
Advisors/Committee Members: Storch, Judith (chair), Watford, Malcolm (internal member), Anthony, Tracy G. (internal member), Henderson, Greg (outside member), School of Graduate Studies.
Subjects/Keywords: Nutritional Sciences; Metabolism – Regulation; Obesity; Musculoskeletal system
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APA ·
Chicago ·
MLA ·
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CSE |
Export
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Manager
APA (6th Edition):
Xu, Heli, 1. (2019). Fat and fit: metabolic changes in skeletal muscle of liver fatty acid-binding protein knockout mice. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/61041/
Chicago Manual of Style (16th Edition):
Xu, Heli, 1991-. “Fat and fit: metabolic changes in skeletal muscle of liver fatty acid-binding protein knockout mice.” 2019. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/61041/.
MLA Handbook (7th Edition):
Xu, Heli, 1991-. “Fat and fit: metabolic changes in skeletal muscle of liver fatty acid-binding protein knockout mice.” 2019. Web. 18 Jan 2021.
Vancouver:
Xu, Heli 1. Fat and fit: metabolic changes in skeletal muscle of liver fatty acid-binding protein knockout mice. [Internet] [Doctoral dissertation]. Rutgers University; 2019. [cited 2021 Jan 18].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/61041/.
Council of Science Editors:
Xu, Heli 1. Fat and fit: metabolic changes in skeletal muscle of liver fatty acid-binding protein knockout mice. [Doctoral Dissertation]. Rutgers University; 2019. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/61041/
. 
Open Access Theses and Dissertations
