+publisher:"Rutgers University" +contributor:("Bello, Nicholas T")

Rutgers University

1. Krumm, Elizabeth Ann, 1991-. Effects of flame retardants on arcuate gene expression and energy homeostasis in mice.

Degree: MS, Endocrinology and Animal Biosciences, 2015, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/48547/

► Flame retardants (FR), including polybrominated diphenyl ethers (PBDE) congener 2,2’,4,4’tetrabromodiphenyl ether (BDE-47) and organophosphate FR (OPFR) are ubiquitous in the environment and interact with multiple… (more)

▼ Flame retardants (FR), including polybrominated diphenyl ethers (PBDE) congener 2,2’,4,4’tetrabromodiphenyl ether (BDE-47) and organophosphate FR (OPFR) are ubiquitous in the environment and interact with multiple target receptors, including estrogen receptors (ERs). Estrogenic endocrine disruptors (EDCs) such as bisphenol A (BPA) affect reproduction and energy homeostasis and modulate hypothalamic functions including gene expression. Developmental exposures to EDCs also alter offspring energy homeostasis, although little is known about the effects of FR, especially OPFR. Therefore, we investigated if exposure to FR alters genes in arcuate nucleus (ARC) that are known to be regulated by 17-β estradiol (E2) through classical ER in adults and if developmental exposures to FR elicit negative energy balance in adulthood. In Experiment 1, adult male and female mice were orally dosed daily vehicle (oil), 17-α- ethinyl estradiol (2.5 μg/kg) as a positive control, BDE-47 low or high dose (1 mg/kg or 10 mg/kg), and OPFR mixture low or high dose (1 mg/kg or 10 mg/kg of tris (1,3-dichloro-2-propyl) phosphate (TDCPP), triphenyl phosphate (TPP), and tricresyl phosphate (TCP) each) for 28 days. ARC mRNA expression, weekly cumulative body weight gain, and female uteri were measured. In Experiment 2, pregnant female mice were fed vehicle, BDE-47 (1mg/kg), and OPFR mixture (1mg/kg) from gestational day 7 (GD7) to postnatal day (PND) 14. Neonatal pup body weight, anogenital distance (AGD), and sex ratio were measured. Weanlings were fed normal or high-fat diet (ND or HFD) and body weights and food intake were measured weekly until PND140. Adults were tested for body composition, metabolic parameters, and glucose homeostasis. While FR altered E2-regulated ARC gene expression in both sexes, there were more striking effects of FR on males. FR amplify effects of HFD, but also promote negative energy balance when given ND in males. In females, FR increased effects of HFD on body weight gain. These data suggest that these FR alter ARC homeostatic gene expression and energy balance in sex-dependent manner. Advisors/Committee Members: Roepke, Troy Adam (chair), Bello, Nicholas T (internal member), Uzumcu, Mehmet (internal member).

Subjects/Keywords: Fireproofing agents; Gene expression

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APA (6^th Edition):

Krumm, Elizabeth Ann, 1. (2015). Effects of flame retardants on arcuate gene expression and energy homeostasis in mice. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/48547/

Chicago Manual of Style (16^th Edition):

Krumm, Elizabeth Ann, 1991-. “Effects of flame retardants on arcuate gene expression and energy homeostasis in mice.” 2015. Masters Thesis, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/48547/.

MLA Handbook (7^th Edition):

Krumm, Elizabeth Ann, 1991-. “Effects of flame retardants on arcuate gene expression and energy homeostasis in mice.” 2015. Web. 18 Jan 2021.

Vancouver:

Krumm, Elizabeth Ann 1. Effects of flame retardants on arcuate gene expression and energy homeostasis in mice. [Internet] [Masters thesis]. Rutgers University; 2015. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/48547/.

Council of Science Editors:

Krumm, Elizabeth Ann 1. Effects of flame retardants on arcuate gene expression and energy homeostasis in mice. [Masters Thesis]. Rutgers University; 2015. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/48547/

Rutgers University

2. Verpeut, Jessica Lynn, 1987-. Neural behavioral outcomes of a ketogenic diet in engrailed-2 null male mice.

Degree: PhD, Endocrinology and Animal Biosciences, 2015, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/48708/

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A ketogenic diet (KD), high in fat and low in carbohydrates, reduces seizure activity in pediatric epilepsy and improves autistic-related behaviors, but the neural mechanisms… (more)

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A ketogenic diet (KD), high in fat and low in carbohydrates, reduces seizure activity in pediatric epilepsy and improves autistic-related behaviors, but the neural mechanisms involved in these improvements are unknown. In the following studies Engrailed-2 (En2) knockout (KO, En2-/-) and wild-type (WT) male mice were fed either a KD or control diet (CD) from postnatal day (PND) 21 to PND 60 (childhood to young adulthood). We hypothesized that a KD fed during this critical time period would alter biogenic amine concentration, metabolism, behavioral deficits, and ultimately neural activation in En2-/- mice. Biogenic amine levels of norepinephrine (NE), dopamine (DA), and serotonin (5-HT) were reduced in forebrain regions and increased in the cerebellum of KO mice, consistent with previous findings. A KD increased hypothalamic NE in WT mice, but not in KO mice. Social behaviors, i.e. frontal contact, were increased and repetitive grooming behaviors reduced in KO-KD. Regardless of previous diet, KO mice displayed increased chow intake post-restraint stress, indicative of a coping response. A KD restored body weight in KO mice by increasing lean mass to WT-KD, but also increased fat mass. KO-KD had enhanced fat metabolism, increased blood glucose response, and reduced blood pressure. KO-KD exposed to a stranger mouse had increased c-Fos immunoreactivity in the cingulate cortex, septal region, and paraventricular nucleus of the hypothalamus (PVN). KO-CD spent more time interacting with a novel object and had increased c-Fos immunoreactivity in the bed nucleus of the stria terminalis (BNST) and PVN. The unique activation of the cingulate and septal region in KO-KD with exposure to a stranger mouse, suggests that these areas could be critical for social behaviors. This research has implications for understanding the impact of a KD on neural development and autistic-like behaviors.

Advisors/Committee Members: Bello, Nicholas T (chair), Cohick, Wendie (internal member), Roepke, Troy (internal member), Graziano, Michael (outside member).

Subjects/Keywords: Ketogenic diet

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APA (6^th Edition):

Verpeut, Jessica Lynn, 1. (2015). Neural behavioral outcomes of a ketogenic diet in engrailed-2 null male mice. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/48708/

Chicago Manual of Style (16^th Edition):

Verpeut, Jessica Lynn, 1987-. “Neural behavioral outcomes of a ketogenic diet in engrailed-2 null male mice.” 2015. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/48708/.

MLA Handbook (7^th Edition):

Verpeut, Jessica Lynn, 1987-. “Neural behavioral outcomes of a ketogenic diet in engrailed-2 null male mice.” 2015. Web. 18 Jan 2021.

Vancouver:

Verpeut, Jessica Lynn 1. Neural behavioral outcomes of a ketogenic diet in engrailed-2 null male mice. [Internet] [Doctoral dissertation]. Rutgers University; 2015. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/48708/.

Council of Science Editors:

Verpeut, Jessica Lynn 1. Neural behavioral outcomes of a ketogenic diet in engrailed-2 null male mice. [Doctoral Dissertation]. Rutgers University; 2015. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/48708/

Rutgers University

3. Mamounis, Kyle J., 1984-. The metabolic effects of linoleic acid versus saturated fat in male mice, female mice, and offspring exposed maternally.

Degree: PhD, Nutritional Sciences, 2017, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/53693/

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The obesity epidemic is receiving research attention, but that attention may be targeted incorrectly. The biggest change in American diet during the 20th century was… (more)

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The obesity epidemic is receiving research attention, but that attention may be targeted incorrectly. The biggest change in American diet during the 20th century was a replacement of saturated and monounsaturated fats with linoleic acid in the form of industrial seed oils. In order to determine whether fatty acid profile is important for producing obesity I fed wild-type C57BL6/J mice high-fat diets with either high concentrations of saturated fat or linoleic acid. In addition to body weight, I performed metabolic assays and collected hypothalamic tissue for measuring gene expression, targeting the mechanism of hypothalamic inflammation. These experimental diets were fed to in males, ovariectomized females with and without estrogen treatment, and to breeder dams to expose their offspring prenatally. I found that in males, linoleic acid contributed to a small but significant increase in body weight compared to saturated fat, but that all high-fat diets produced obese mice. The biggest difference between groups was insulin resistance in the linoleic acid-fed mice. Gene expression evidence of hypothalamic inflammation was unclear. In female mice, estrogen conferred protection from obesity caused by all experimental high-fat diets. Without estrogen, female mice were equally obese from saturated fat and linoleic acid. Glucose metabolism, however, was also impaired by linoleic acid, and expression of hypothalamic genes for metabolism and inflammation were highly variable. In offspring exposed to maternal high-fat diet, females were again protected but not males. Male mice weaned onto a high-fat diet gained more weight when exposed to linoleic acid through maternal feeding than saturated fat. A similar effect on glucose metabolism was seen in male and female offspring as in the first two experiments, where linoleic acid feeding impaired glucose clearance during glucose or insulin challenge. My conclusion is that, in the mouse, linoleic acid is slightly more obesogenic than saturated fat, but effects glucose metabolism much more potently. The effects on obesity, but not glycemia, are partially protected in female mice by estrogen. Due to a lack of clear hypothalamic inflammation biomarkers, these effects are likely occurring in the periphery.

Advisors/Committee Members: Roepke, Troy A (chair), Bello, Nicholas T (internal member), Campbell, Sara C (internal member), Storch, Judith (internal member), Cai, Dongsheng (outside member).

Subjects/Keywords: Linoleic acid; Obesity

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APA (6^th Edition):

Mamounis, Kyle J., 1. (2017). The metabolic effects of linoleic acid versus saturated fat in male mice, female mice, and offspring exposed maternally. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/53693/

Chicago Manual of Style (16^th Edition):

Mamounis, Kyle J., 1984-. “The metabolic effects of linoleic acid versus saturated fat in male mice, female mice, and offspring exposed maternally.” 2017. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/53693/.

MLA Handbook (7^th Edition):

Mamounis, Kyle J., 1984-. “The metabolic effects of linoleic acid versus saturated fat in male mice, female mice, and offspring exposed maternally.” 2017. Web. 18 Jan 2021.

Vancouver:

Mamounis, Kyle J. 1. The metabolic effects of linoleic acid versus saturated fat in male mice, female mice, and offspring exposed maternally. [Internet] [Doctoral dissertation]. Rutgers University; 2017. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/53693/.

Council of Science Editors:

Mamounis, Kyle J. 1. The metabolic effects of linoleic acid versus saturated fat in male mice, female mice, and offspring exposed maternally. [Doctoral Dissertation]. Rutgers University; 2017. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/53693/

Rutgers University

4. Wang, Yang, 1989-. Effects of high fat feeding and dietary vitamin D on calcium, bone, and vitamin D metabolism in mature mice.

Degree: PhD, Nutritional Sciences, 2017, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/54036/

► Dietary fat sources containing high caloric energy are closely linked to energy overconsumption induced obesity leading to a variety of health problems, including compromised bone… (more)

▼ Dietary fat sources containing high caloric energy are closely linked to energy overconsumption induced obesity leading to a variety of health problems, including compromised bone quality. High fat diets (HFD) also affect calcium metabolism. However, effects of HFD on intestinal calcium absorption and bone health in mature animals have not been addressed, and different types of dietary fatty acids may have differential effects (e.g. monounsaturated fatty acids (MUFA) vs. saturated fatty acids (SFA). In addition, low circulating vitamin D status is commonly found in obese individuals. However, the nature of the association between vitamin D deficiency and obesity remains unclear because an underlying mechanism for the association has not been delineated. Therefore, in the current dissertation, we sought to reveal the effects of dietary fat and vitamin D intake on calcium and vitamin D metabolism and bone health using a mature mouse model. In study 1, the effects of HFD enriched with MUFA or with SFA on intestinal calcium absorption and bone health in mature lean mice were investigated. C57BL/6J mice were weight-controlled fed with either 10% normal fat diet (NFD) or a HFD (45% fat) enriched with either MUFA or SFA for 10wk. We found that high compared with normal fat intake induced higher fractional Ca absorption (Ca45 isotope method) and this did not differ with the type of dietary fatty acids (MUFA vs. SFA). In contrast, only the high fat feeding with SFA adversely affected total and femoral area bone mineral density (dual-energy X-ray absorptiometry), while MUFA was associated with greater femoral trabecular bone volume fraction (BV/TV) and thickness (micro-computerized tomography system). In study 2, the objective was to determine whether high MUFA intake would have a neutral or even a beneficial effect on mature bone health under conditions of excess caloric intake and obesity, and whether high MUFA and SFA feeding would differentially affect vitamin D metabolism in obese mice. After ad libitum feeding C57BL/6J mice 10% NFD or 45% HFD enriched with MUFA or SFA for 10wk, we found that the HFD enriched with SFA, but not MUFA, resulted in greater energy intake, weight gain, total body fat mass (EchoMRI Body Composition Analyzer), and liver fat. High SFA intake, but not MUFA, also adversely affected femoral trabecular bone parameters, though no detrimental effects of SFA on bone mass were seen in mature mice under the condition of excess caloric intake and obesity. Moreover, high fat feeding lowered circulating 25OHD concentration (ELISA), which was also inversely associated with body fat percentage. However, this finding was not explained by differential effects of MUFA and SFA on gene (rt-PCR) and protein (western blotting) expression of hepatic vitamin D 25-hydroxylase Cyp2r1 in mature mice. In study 3, the aim was to determine effects of dietary vitamin D on food intake and adiposity with and without high fat feeding. We found that supplemental vitamin D showed no beneficial effects on preventing HFD-induced… Advisors/Committee Members: Miller, Joshua W (chair), Shapses, Sue A (co-chair), Watford, Malcolm (internal member), Bello, Nicholas T (internal member), Buckendahl, Patricia (outside member).

Subjects/Keywords: Nutrition; Vitamin D

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

APA (6^th Edition):

Wang, Yang, 1. (2017). Effects of high fat feeding and dietary vitamin D on calcium, bone, and vitamin D metabolism in mature mice. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/54036/

Chicago Manual of Style (16^th Edition):

Wang, Yang, 1989-. “Effects of high fat feeding and dietary vitamin D on calcium, bone, and vitamin D metabolism in mature mice.” 2017. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/54036/.

MLA Handbook (7^th Edition):

Wang, Yang, 1989-. “Effects of high fat feeding and dietary vitamin D on calcium, bone, and vitamin D metabolism in mature mice.” 2017. Web. 18 Jan 2021.

Vancouver:

Wang, Yang 1. Effects of high fat feeding and dietary vitamin D on calcium, bone, and vitamin D metabolism in mature mice. [Internet] [Doctoral dissertation]. Rutgers University; 2017. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/54036/.

Council of Science Editors:

Wang, Yang 1. Effects of high fat feeding and dietary vitamin D on calcium, bone, and vitamin D metabolism in mature mice. [Doctoral Dissertation]. Rutgers University; 2017. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/54036/

Rutgers University

5. 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… (more)

▼ 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 (6^th 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 (16^th 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 (7^th 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/

6. Gotthardt, Juliet D. The metabolic, neural, and behavioral outcomes of intermittent caloric deprivation in diet-induced obese mice.

Degree: PhD, Nutritional Sciences, 2017, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/55479/

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Alternate day intermittent fasting (IMF) has recently gained traction as a popular dietary strategy to produce weight loss in obese individuals. In this dissertation, we… (more)

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Alternate day intermittent fasting (IMF) has recently gained traction as a popular dietary strategy to produce weight loss in obese individuals. In this dissertation, we investigate the metabolic, neural, and behavioral effects of IMF to further elucidate the mechanisms driving sustained weight loss. To produce diet-induced obesity, male mice were placed on an ad libitum 45% high fat diet (HFD) for 8 weeks. Animals were subsequently placed on one of four experimental diets for 4 weeks as follows: continuation of ad libitum HFD, IMF of HFD (IMF-HFD), switched to a 10% low fat diet (LFD), or IMF of LFD (IMF-LFD). IMF-HFD and IMF-LFD animals consistently lost body weight, 13-27% and 18-32% reduction respectively, compared to HFD animals. Oral glucose tolerance AUC was lower in IMF-HFD (~50%) while insulin tolerance AUC was reduced in IMF-HFD, LFD, and IMF-LFD (~22-42%). Norepinephrine content in the anterior portion of the medial hypothalamus was higher in IMF animals compared to HFD and LFD groups while only IMF-LFD was higher in the posterior portion. Furthermore, relative Npy gene expression was higher in IMF-HFD and IMF-LFD compared to HFD and LFD mice. Neural activation of hypothalamic NPY neurons was measured following an acute glucoprivic challenge with 2-deoxy-D-glucose (2-DG). In the paraventricular nucleus, there was a significant increase in neural activation following 2-DG administration, but there were no differences between treatment groups given 2-DG. There were no differences in the arcuate nucleus nor were there differences in NPY/c-Fos double-labeling in either region. A subset of animals, which also including groups pair-fed to IMF animals (PF-HFD and PF-LFD) were used to evaluate feeding behavior during IMF and after 6 weeks of HFD re-feeding. At the end of the diet period, the first meal of the last feeding day was recorded. The first meal duration was longer in LFD and IMF-LFD mice compared to HFD. Additionally, IMF-HFD had a greater first meal size and faster rate of consumption than HFD animals. Average meal duration at the end of the diet period was longer in the low-fat diet groups compared to the HFD-groups. There were no meal pattern differences at the end of the HFD re-feeding period. In summary, these results suggest that IMF is an effective strategy for weight loss that produces specific alterations in hypothalamic signaling and that meal patterns are only transiently altered in diet-induced obese male mice.

Advisors/Committee Members: Bello, Nicholas T (chair), Roepke, Troy A (internal member), Shapses, Sue A (internal member), Varady, Krista A (outside member), School of Graduate Studies.

Subjects/Keywords: Intermittent fasting

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APA (6^th Edition):

Gotthardt, J. D. (2017). The metabolic, neural, and behavioral outcomes of intermittent caloric deprivation in diet-induced obese mice. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/55479/

Chicago Manual of Style (16^th Edition):

Gotthardt, Juliet D. “The metabolic, neural, and behavioral outcomes of intermittent caloric deprivation in diet-induced obese mice.” 2017. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/55479/.

MLA Handbook (7^th Edition):

Gotthardt, Juliet D. “The metabolic, neural, and behavioral outcomes of intermittent caloric deprivation in diet-induced obese mice.” 2017. Web. 18 Jan 2021.

Vancouver:

Gotthardt JD. The metabolic, neural, and behavioral outcomes of intermittent caloric deprivation in diet-induced obese mice. [Internet] [Doctoral dissertation]. Rutgers University; 2017. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/55479/.

Council of Science Editors:

Gotthardt JD. The metabolic, neural, and behavioral outcomes of intermittent caloric deprivation in diet-induced obese mice. [Doctoral Dissertation]. Rutgers University; 2017. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/55479/

Rutgers University

7. Skorupa, Jennifer A., 1990-. IGFBP-3 induced by ribotoxic stress is not secreted prior to nuclear localization in mammary epithelial cells.

Degree: MS, Endocrinology and Animal Biosciences, 2018, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/56124/

► Ribotoxic stressors such as anisomycin (ANS) and deoxynivalenol (DON) induce apoptosis in MAC-T cells. These agents also increase IGFBP-3 expression and knockdown of IGFBP-3 mitigates… (more)

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APA (6^th Edition):

Skorupa, Jennifer A., 1. (2018). IGFBP-3 induced by ribotoxic stress is not secreted prior to nuclear localization in mammary epithelial cells. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/56124/

Chicago Manual of Style (16^th Edition):

Skorupa, Jennifer A., 1990-. “IGFBP-3 induced by ribotoxic stress is not secreted prior to nuclear localization in mammary epithelial cells.” 2018. Masters Thesis, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/56124/.

MLA Handbook (7^th Edition):

Skorupa, Jennifer A., 1990-. “IGFBP-3 induced by ribotoxic stress is not secreted prior to nuclear localization in mammary epithelial cells.” 2018. Web. 18 Jan 2021.

Vancouver:

Skorupa, Jennifer A. 1. IGFBP-3 induced by ribotoxic stress is not secreted prior to nuclear localization in mammary epithelial cells. [Internet] [Masters thesis]. Rutgers University; 2018. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/56124/.

Council of Science Editors:

Skorupa, Jennifer A. 1. IGFBP-3 induced by ribotoxic stress is not secreted prior to nuclear localization in mammary epithelial cells. [Masters Thesis]. Rutgers University; 2018. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/56124/

Rutgers University

8. Cabrera, Miguel Alexander. Fetal alcohol exposure induces neurotoxic effects on β-endorphin neurons through microglial activation.

Degree: PhD, Endocrinology and Animal Biosciences, 2018, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/58931/

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Fetal alcohol exposure has many detrimental effects on the developing brain and can cause fetal alcohol spectrum disorders (FASDs). Many FASDs patients show lifelong stress… (more)

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Fetal alcohol exposure has many detrimental effects on the developing brain and can cause fetal alcohol spectrum disorders (FASDs). Many FASDs patients show lifelong stress response abnormalities, demonstrated by an augmented response to stress hormones such as adrenocorticotropin and corticosterone (Lee et al., 2000), which are likely driven by alterations the hypothalamic-pituitary-adrenal (HPA) axis function (Zhang et al., 2005). Using a rat animal model, we have shown that postnatal ethanol exposure reduces the number and function of stress regulatory β-endorphin producing neurons in the hypothalamus, inducing a hyper-stress response (Sarkar et al., 2007; Logan et al., 2015). Microglia are one of the innate immune cells in the CNS and can be categorized as activated or ramified. Activated microglia are associated with an increase in proinflammatory responses and phagocytosis while ramified microglia are associated with maintaining homeostasis through dynamic communication, remodeling of neuronal synapses, and surveying the environment (Bell-Temin et al., 2013). How β-endorphin neurons communicate with microglia to maintain normal homeostasis has yet to be addressed. β-endorphin can also bind to both mu- and delta-opioid receptors and may serve as a form of communication between β-endorphin neurons and microglia. Exosomes are small vesicles (30-150 nm) that play an important role in local and distant communication between cells. They carry unique cargo (proteins, mRNA, miRNA, and other non-coding RNAs) from the cells they originate from that can affect the recipient cell’s homeostasis and induce apoptosis. Additionally, complement proteins, generally known for their role to opsonize foreign pathogens and support phagocytosis of dying cells may also play a role in ethanol-induced β-endorphin neuronal cell death. Here I demonstrate that ethanol-induced apoptosis of β-endorphin neurons is caused by activation of microglia to release proinflammatory cytokines, pro-apoptotic exosomes, and C1q. Furthermore, mu-opioid receptors activation is critical to ethanol-induced activation of microglia to induce apoptosis of β-endorphin neurons and antagonism of mu-opioid receptors attenuated the ethanol effect. Delta-opioid receptors antagonism did not have an effect on ethanol-induced β-endorphin neuronal cell death.

Advisors/Committee Members: Sarkar, Dipak K (chair), Roepke, Troy A (internal member), Bello, Nicholas T (internal member), Wu, Longjun (outside member), School of Graduate Studies.

Subjects/Keywords: Fetal alcohol spectrum disorders

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APA (6^th Edition):

Cabrera, M. A. (2018). Fetal alcohol exposure induces neurotoxic effects on β-endorphin neurons through microglial activation. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/58931/

Chicago Manual of Style (16^th Edition):

Cabrera, Miguel Alexander. “Fetal alcohol exposure induces neurotoxic effects on β-endorphin neurons through microglial activation.” 2018. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/58931/.

MLA Handbook (7^th Edition):

Cabrera, Miguel Alexander. “Fetal alcohol exposure induces neurotoxic effects on β-endorphin neurons through microglial activation.” 2018. Web. 18 Jan 2021.

Vancouver:

Cabrera MA. Fetal alcohol exposure induces neurotoxic effects on β-endorphin neurons through microglial activation. [Internet] [Doctoral dissertation]. Rutgers University; 2018. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/58931/.

Council of Science Editors:

Cabrera MA. Fetal alcohol exposure induces neurotoxic effects on β-endorphin neurons through microglial activation. [Doctoral Dissertation]. Rutgers University; 2018. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/58931/

Rutgers University

9. 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)

Subjects/Keywords: Dietary sulfur amino acid restriction; ATF4

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APA (6^th 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 (16^th 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 (7^th 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

10. Kreitman, Alexandra, 1995-. Bone turnover and GLP-1 respond to a putative α-glucosidase inhibitor.

Degree: MS, Nutritional Sciences, 2019, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/61784/

► The botanical, Salacia chinensis (SC), has α-glucosidase inhibitor (α-GI) properties that attenuates postprandial glycemic indices and increases secretion of glucagon-like peptide (GLP-1), a gut peptide… (more)

Subjects/Keywords: GLP-1; Glucagon-like peptide 1; Glucosidase inhibitors

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

APA (6^th Edition):

Kreitman, Alexandra, 1. (2019). Bone turnover and GLP-1 respond to a putative α-glucosidase inhibitor. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/61784/

Chicago Manual of Style (16^th Edition):

Kreitman, Alexandra, 1995-. “Bone turnover and GLP-1 respond to a putative α-glucosidase inhibitor.” 2019. Masters Thesis, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/61784/.

MLA Handbook (7^th Edition):

Kreitman, Alexandra, 1995-. “Bone turnover and GLP-1 respond to a putative α-glucosidase inhibitor.” 2019. Web. 18 Jan 2021.

Vancouver:

Kreitman, Alexandra 1. Bone turnover and GLP-1 respond to a putative α-glucosidase inhibitor. [Internet] [Masters thesis]. Rutgers University; 2019. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/61784/.

Council of Science Editors:

Kreitman, Alexandra 1. Bone turnover and GLP-1 respond to a putative α-glucosidase inhibitor. [Masters Thesis]. Rutgers University; 2019. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/61784/

Rutgers University

11. Yasrebi, Ali, 1987-. ERE-independent ERα signalling in feeding and exploratory behaviors.

Degree: MS, Endocrinology and Animal Biosciences, 2019, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/62067/

► The reproductive steroid hormone, 17β-estradiol (E2), controls feeding and exploratory behaviors associated with mood disorders. The loss of circulating E2 puts menopausal women at an… (more)

▼ The reproductive steroid hormone, 17β-estradiol (E2), controls feeding and exploratory behaviors associated with mood disorders. The loss of circulating E2 puts menopausal women at an increased risk for developing obesity and mood disorders when compared to premenopausal women. Therefore, it is critically important to understand the role of sex steroids and their receptors in the neuroendocrine control of feeding and mood. The goal of this project is to understand the role of estrogen response Element (ERE)-dependent and ERE-independent ERα signaling on behavior by characterizing feeding patters and exploratory behaviors in male and female mice lacking either total ERα signaling or lacking ERE-dependent ERα signaling. We hypothesize that ERE-independent ERα is partially sufficient to restore feeding and exploratory behaviors that are lost in total ERα knockout mice. We tested three strains of mice: two ERα transgenic models, a total ERα knock out (ERKO) and a novel ERα knock in/knock out (KIKO) that lacks a functional DNA-binding domain) and their wild type (WT) C57 littermates using a real-time feeding behavior monitoring system and series of standard behavior tests (open field tests, elevated plus maze, forced swim test). To test our hypothesis FI and meal patterns were observed while the animals were given ad libitum access to a LFD (Experiment 1a) followed by HFD (Experiment 1b). A separate set of animals the response to fasting was monitored for 24 h after caloric restriction (Experiment 1c). Exploratory, depressive, and locomotor behavior testing was conducted on mice from Experiments 1a/b (open field, elevated plus maze, forced swim test). Each experiment was initially done with intact animals and then again repeated in ovariectomized (OVX) animals split into either an oil treated control group or an E2-treated group. We observed ERE-dependent mechanisms are the main modulator of homeostatic LFD feeding meal patterns while ERE- independent ERα signaling was involved in the control of palatable, high-fat diet food intake. During refeeding, ERE-independent mechanisms contribute to a decreased first meal food intake and slower rate of ingestion. When observed during a series of behavior tests, WT animals explored more, regardless of treatment (differences could be attributed to higher levels of locomotor activity in WT). However, similarities between WT and KIKO females in the EPM indicate that ERE-independent pathways may contribute towards reducing anxiety measures, independent of locomotor activity. WT females were shown to have a decreased free float time, indicating ERE dependent signaling may be influencing despair like tendencies. Collectively, these suggest that both ERE-dependent and -independent ERαsignaling are involved with both feeding and anxiety like homeostatic parameters. Advisors/Committee Members: Roepke, Troy A (chair), Bello, Nicholas T (internal member), Bagnell, Carol A (internal member), Samuels, Benjamin A (outside member), School of Graduate Studies.

Subjects/Keywords: Estrogen receptor alpha; Estrogen – Receptors

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

APA (6^th Edition):

Yasrebi, Ali, 1. (2019). ERE-independent ERα signalling in feeding and exploratory behaviors. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/62067/

Chicago Manual of Style (16^th Edition):

Yasrebi, Ali, 1987-. “ERE-independent ERα signalling in feeding and exploratory behaviors.” 2019. Masters Thesis, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/62067/.

MLA Handbook (7^th Edition):

Yasrebi, Ali, 1987-. “ERE-independent ERα signalling in feeding and exploratory behaviors.” 2019. Web. 18 Jan 2021.

Vancouver:

Yasrebi, Ali 1. ERE-independent ERα signalling in feeding and exploratory behaviors. [Internet] [Masters thesis]. Rutgers University; 2019. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/62067/.

Council of Science Editors:

Yasrebi, Ali 1. ERE-independent ERα signalling in feeding and exploratory behaviors. [Masters Thesis]. Rutgers University; 2019. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/62067/

Rutgers University

12. Burgess, Brenda, 1988-. The PROP bitter taste phenotype associates with weight loss and changes in liking for sweet and savory-fat foods in women in a lifestyle intervention.

Degree: PhD, Nutritional Sciences, 2016, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/51238/

►

Behavioral weight loss interventions are effective at achieving clinically significant weight loss, though weight regain is common because dietary adherence is problematic. Studies report that… (more)

▼

Behavioral weight loss interventions are effective at achieving clinically significant weight loss, though weight regain is common because dietary adherence is problematic. Studies report that taste is the primary determinant of food intake, so accounting for individual variability in taste preferences may improve adherence to a weight loss regimen. Genetically mediated sensitivity to the bitter compound, 6-n-propylthiouracil (PROP) associates with differences in perception and preference for basic tastes and oral textures, most notably fat. Previous research from our laboratory has revealed that PROP non-taster (NT) women exhibit higher preferences for, and daily intake of, fat when compared to PROP super-taster (ST) women, suggesting that a single dietary approach may not be appropriate for everyone attempting to lose weight. In our study, we randomized PROP ST and NT women with obesity to a low-fat (LF) or low-carbohydrate (LC) diet within a 6-month behavioral weight loss intervention to assess whether prescribing a diet complementary to their taste preferences would improve dietary adherence to promote greater weight loss. As an ancillary study, we investigated whether changes in taste perception and liking for sweet and fatty foods would occur concomitantly with weight loss throughout the intervention. For the main study, results showed that PROP NT women randomized to the LC diet lost more weight than NT women randomized to the LF diet (-8.5 Â± 0.5 kg vs. -6.6 Â± 0.5 kg, P = 0.008), and that weight loss was comparable for ST women randomized to either diet (-8.9 Â± 0.5 vs. -8.8 Â± 0.4, P = 0.35). Dietary analyses indicated that energy and fat intake were consistent with the dietary prescriptions, though were not associated to weight loss. These findings suggest that pre-screening for PROP status may be an effective tool for improving weight loss outcomes in women, but further research is necessary to understand the dietary patterns of NT and ST women within a weight loss context. For the ancillary study, analyses detected a change in liking, but not perception, for sweet and fatty foods. By 6 months, liking increased for tasted foods with less sugar and fat, irrespective of diet. These findings show that gradual weight loss is capable of modifying taste preferences, which could serve to influence food selection patterns and be implicated in weight loss maintenance.

Advisors/Committee Members: Byrd-Bredbenner, Carol (internal member), Tepper, Beverly J (internal member), Bello, Nicholas T (internal member), Shapses, Sue A (internal member), Raynor, Hollie A (outside member).

Subjects/Keywords: Phenotype; Weight loss

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

APA (6^th Edition):

Burgess, Brenda, 1. (2016). The PROP bitter taste phenotype associates with weight loss and changes in liking for sweet and savory-fat foods in women in a lifestyle intervention. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/51238/

Chicago Manual of Style (16^th Edition):

Burgess, Brenda, 1988-. “The PROP bitter taste phenotype associates with weight loss and changes in liking for sweet and savory-fat foods in women in a lifestyle intervention.” 2016. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/51238/.

MLA Handbook (7^th Edition):

Burgess, Brenda, 1988-. “The PROP bitter taste phenotype associates with weight loss and changes in liking for sweet and savory-fat foods in women in a lifestyle intervention.” 2016. Web. 18 Jan 2021.

Vancouver:

Burgess, Brenda 1. The PROP bitter taste phenotype associates with weight loss and changes in liking for sweet and savory-fat foods in women in a lifestyle intervention. [Internet] [Doctoral dissertation]. Rutgers University; 2016. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/51238/.

Council of Science Editors:

Burgess, Brenda 1. The PROP bitter taste phenotype associates with weight loss and changes in liking for sweet and savory-fat foods in women in a lifestyle intervention. [Doctoral Dissertation]. Rutgers University; 2016. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/51238/

Rutgers University

13. Olson, Ryan L. Exercise as a neurobehavioral therapy for cognitive control deficits in major depressive disorder.

Degree: PhD, Nutritional Sciences, 2016, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/51389/

►

Major depressive disorder (MDD) is associated with a number of symptoms, including cognitive dysfunction and maladaptive ruminative thought patterns. Although consistent evidence indicates that aerobic… (more)

▼

Major depressive disorder (MDD) is associated with a number of symptoms, including cognitive dysfunction and maladaptive ruminative thought patterns. Although consistent evidence indicates that aerobic exercise is beneficial for reducing depressive symptoms in MDD, little is known about the influence of exercise on neurocognitive deficits found in depression. This is important for establishing exercise as a neurobehavioral therapy for depression, that is, an intervention that addresses biological mechanisms believed to underlie the disorder. Here, we investigated whether the N2 and P3 components of the human event-related potential (ERP) could be used to index cognitive impairments in MDD, and whether these neurophysiological measures were correlated with ruminative thought patterns. Although there were no differences in P3 amplitude by depression status, N2 amplitudes were significantly reduced in individuals with MDD relative to healthy controls, indicating that reductions were associated with higher rumination levels. These findings demonstrate that individuals with MDD may experience impaired cognitive control while attending to varying environmental stimuli. Because of our findings related to impaired cognitive control processes, we examined the neurophysiological and behavioral correlates of cognitive control during single bouts of low- and moderate-intensity exercise in healthy young adults to determine if neurocognitive function is modifiable by aerobic exercise. Importantly, acute exercise was shown to modify these ERP components, such that increased N2 and P3 amplitudes were found during exercise at low and moderate intensities relative to rest. Although this study was performed in nondepressed participants, it suggests an upregulation of cognitive control during aerobic exercise that may be maintained through a program of chronic exercise. Finally, we examined the effects of a moderate-intensity aerobic exercise intervention performed three days/week for 8 weeks. The aerobic exercise condition exhibited enhanced cognitive control (i.e., N2 amplitude) and reduced depressive symptoms among individuals with MDD; however, these exercise-induced changes in cognitive control were not found to significantly mediate pre-to-post changes in symptom outcomes. These findings support the use of exercise as a neurobehavioral therapy for MDD and suggest the possibility of incorporating exercise as a stand alone or augmentation strategy for conventional treatments.

Advisors/Committee Members: Alderman, Brandon L (chair), Bello, Nicholas T (internal member), Shapses, Sue A (internal member), Campbell, Sara C (internal member), Shors, Tracey J (outside member).

Subjects/Keywords: Depressive disorder – Treatment; Depression, Mental – Treatment; Exercise

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

APA (6^th Edition):

Olson, R. L. (2016). Exercise as a neurobehavioral therapy for cognitive control deficits in major depressive disorder. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/51389/

Chicago Manual of Style (16^th Edition):

Olson, Ryan L. “Exercise as a neurobehavioral therapy for cognitive control deficits in major depressive disorder.” 2016. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/51389/.

MLA Handbook (7^th Edition):

Olson, Ryan L. “Exercise as a neurobehavioral therapy for cognitive control deficits in major depressive disorder.” 2016. Web. 18 Jan 2021.

Vancouver:

Olson RL. Exercise as a neurobehavioral therapy for cognitive control deficits in major depressive disorder. [Internet] [Doctoral dissertation]. Rutgers University; 2016. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/51389/.

Council of Science Editors:

Olson RL. Exercise as a neurobehavioral therapy for cognitive control deficits in major depressive disorder. [Doctoral Dissertation]. Rutgers University; 2016. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/51389/

Rutgers University

14. Murphy, Melissa Anne, 1983-. Discerning the effect of salt, riboflavin and MTHFR on acute blood pressure response.

Degree: PhD, Nutritional Sciences, 2017, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/53956/

►

Problem: Elevated blood pressure (BP) is a top cause of mortality and leads to millions of global deaths each year; yet the cause of general… (more)

▼

Problem: Elevated blood pressure (BP) is a top cause of mortality and leads to millions of global deaths each year; yet the cause of general hypertension (HTN) is not known. Many studies link dietary factors, particularly high sodium levels, with HTN and related cardiovascular diseases. Other studies have identified certain genes, including methylenetetrahydrofolate reductase (MTHFR) involved in folate metabolism, with a greater risk of developing HTN. Hypothesis: These studies sought to identify the impact of MTHFR genotype on the acute BP response to salt ingestion. We hypothesized that individuals would have a greater decrease in BP following salt ingestion compared to water and that this response would be diminished by the MTHFR 677TT variant allele. Methods: In an initial cohort, acute BP response was assessed, multiple times per subject, in a series of time points following an ingestion of salt or water. A secondary cohort was formed of individuals with MTHFR677 genotypes whose BP and blood were collected. Blood samples were analyzed for plasma riboflavin, homocysteine, MTHFR genotype and nitrate/nitrite levels. These data were analyzed for differences in BP response, genotypes, micronutrient status and for associations between subjects’ characteristics and BP response. Results: BP decreases within the first 60 minutes following salt ingestion. When measuring resting BP, no difference was found in BP between MTHFR genotypes. However, individuals with the 677TT variant genotype demonstrated an attenuated acute BP response to salt ingestion compared to individuals with the wild-type 677CC genotype. Conclusions: BP decreases acutely in response to salt ingestion. The MTHFR 677TT variant genotype was not associated with elevated resting BP. However, measuring acute BP response illustrated a limited response in the MTHFR variant genotype compared with the wild-type MTHFR genotype. These findings suggest that acute BP response may be a useful measure of a dynamic system, highlighting characteristics that are risk factors for HTN.

Advisors/Committee Members: Miller, Joshua W. (chair), Breslin, Paul A.S. (co-chair), Shapses, Sue A. (internal member), Bello, Nicholas T. (internal member), Gow, Andrew W. (outside member).

Subjects/Keywords: Blood pressure; Hypertension; Methylenetetrahydrofolate reductase

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

APA (6^th Edition):

Murphy, Melissa Anne, 1. (2017). Discerning the effect of salt, riboflavin and MTHFR on acute blood pressure response. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/53956/

Chicago Manual of Style (16^th Edition):

Murphy, Melissa Anne, 1983-. “Discerning the effect of salt, riboflavin and MTHFR on acute blood pressure response.” 2017. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/53956/.

MLA Handbook (7^th Edition):

Murphy, Melissa Anne, 1983-. “Discerning the effect of salt, riboflavin and MTHFR on acute blood pressure response.” 2017. Web. 18 Jan 2021.

Vancouver:

Murphy, Melissa Anne 1. Discerning the effect of salt, riboflavin and MTHFR on acute blood pressure response. [Internet] [Doctoral dissertation]. Rutgers University; 2017. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/53956/.

Council of Science Editors:

Murphy, Melissa Anne 1. Discerning the effect of salt, riboflavin and MTHFR on acute blood pressure response. [Doctoral Dissertation]. Rutgers University; 2017. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/53956/

Rutgers University

15. Sachdeo, Bryn Leonard, 1985-. Feeding behavioral pharmacogenetics of a murine model of the OPRM1 A118G polymorphism.

Degree: PhD, Nutritional Sciences, 2019, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/61930/

►

Binge eating disorder (BED) is the most prevalent eating disorder, and is characterized by a perceived “loss of control” over ones food intake, resulting in… (more)

▼

Binge eating disorder (BED) is the most prevalent eating disorder, and is characterized by a perceived “loss of control” over ones food intake, resulting in the consumption of large amounts of food in short periods of time. There is currently one FDA-approved drug for the treatment of BED, lisdexamfetamine dimesylate. A common single nucleotide polymorphism (SNP) of the mu-opioid receptor gene (OPRM1 A118G) results in an amino acid substitution (N40D) in the extracellular domain that is posited to alter receptor stability and ligand binding. The OPRM1 A118G SNP has been associated with alterations in nociception and analgesia, as well as altered susceptibility to substance abuse. GG allele status has also been associated with BED in an obese population, as well as increased preference and intake of highly-palatable foods. In this dissertation, an established rodent model of binge-like feeding was utilized to investigate the role of the homologous SNP in mice (OPRM1 A112G; N38D) in binge propensity, pharmacological efficacy, and taste and meal phenotyping in male and female mice. The 6-wk, intermittent 24-hr caloric restriction and/or 30-min subsequent binge access feeding schedules (Restrict, R; Binge, B; Restrict-Binge, RB; Naïve, N) revealed no differences in binge intakes between AA and GG genotypes in male or female mice. Following the 6-wk protocol, female mice underwent acute or chronic dosing schedules: within-group, 1x/wk dosing of vehicle (Veh; water), lisdexamfetamine dimesylate (LDX; 0.15, 0.5, 1.5 mg/kg), and sibutramine hydrochloride (Sib; 0.3, 1.0, 3.0 mg/kg); or between-group, 2-wk daily dosing of either Veh, Sib (3.0 mg/kg), or LDX (1.5 mg/kg), respectively. There was no effect of AA or GG genotype on pharmacotherapeutic efficacy in reducing binge-like feeding. Two-bottle lipid preference tests in male mice previously exposed to the 6-wk feeding schedules revealed increased preference for Intralipid (IL) in R and RB groups compared to N, for 5% IL only, and N GG had lower preference than N AA mice. Genotype differences in brief-access taste responsivity in male and female mice were observed only in sweet, nutritive carbohydrate taste stimuli. There was no effect of genotype on meal microstructure in male mice, but female GG mice had larger average meal sizes and greater total caloric meal intakes. Although there may be some elements of taste and meal patterns mediated by OPRM1 A112G SNP status, our data does not support a role for this common SNP in the predisposition to binge-like feeding nor the efficacy of pharmacotherapy. While the concept of “personalized medicine” remains intriguing, the current studies do not suggest a role for the involvement of the OPRM1 A118G SNP in binge eating disorder.

Advisors/Committee Members: Bello, Nicholas T. (chair), Storch, Judith (internal member), Miller, Joshua (internal member), Pang, Zhiping (outside member), Yu, Lei (outside member), School of Graduate Studies.

Subjects/Keywords: OPRM1 A118G; Compulsive eating – Treatment

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

APA (6^th Edition):

Sachdeo, Bryn Leonard, 1. (2019). Feeding behavioral pharmacogenetics of a murine model of the OPRM1 A118G polymorphism. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/61930/

Chicago Manual of Style (16^th Edition):

Sachdeo, Bryn Leonard, 1985-. “Feeding behavioral pharmacogenetics of a murine model of the OPRM1 A118G polymorphism.” 2019. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/61930/.

MLA Handbook (7^th Edition):

Sachdeo, Bryn Leonard, 1985-. “Feeding behavioral pharmacogenetics of a murine model of the OPRM1 A118G polymorphism.” 2019. Web. 18 Jan 2021.

Vancouver:

Sachdeo, Bryn Leonard 1. Feeding behavioral pharmacogenetics of a murine model of the OPRM1 A118G polymorphism. [Internet] [Doctoral dissertation]. Rutgers University; 2019. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/61930/.

Council of Science Editors:

Sachdeo, Bryn Leonard 1. Feeding behavioral pharmacogenetics of a murine model of the OPRM1 A118G polymorphism. [Doctoral Dissertation]. Rutgers University; 2019. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/61930/

Rutgers University

16. Zhang, Changqing, 1984-. Role of beta-endorphin in control of stress and cancer progression in fetal alcohol exposed rats.

Degree: Animal Sciences, 2013, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/42092/

Subjects/Keywords: Endorphins; Rats – Effect of stress on; Alcohol – Physiological effect; Cancer – Etiology; Cancer in animals

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

APA (6^th Edition):

Zhang, Changqing, 1. (2013). Role of beta-endorphin in control of stress and cancer progression in fetal alcohol exposed rats. (Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/42092/

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

Chicago Manual of Style (16^th Edition):

Zhang, Changqing, 1984-. “Role of beta-endorphin in control of stress and cancer progression in fetal alcohol exposed rats.” 2013. Thesis, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/42092/.

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

MLA Handbook (7^th Edition):

Zhang, Changqing, 1984-. “Role of beta-endorphin in control of stress and cancer progression in fetal alcohol exposed rats.” 2013. Web. 18 Jan 2021.

Vancouver:

Zhang, Changqing 1. Role of beta-endorphin in control of stress and cancer progression in fetal alcohol exposed rats. [Internet] [Thesis]. Rutgers University; 2013. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/42092/.

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

Council of Science Editors:

Zhang, Changqing 1. Role of beta-endorphin in control of stress and cancer progression in fetal alcohol exposed rats. [Thesis]. Rutgers University; 2013. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/42092/

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

Rutgers University

17. Agostini-Dreyer, Allyson M., 1986-. Role of endogenous IGFBP-3 in mammary epithelial cell apoptosis.

Degree: Nutritional Sciences, 2014, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/43942/

Subjects/Keywords: Somatomedin; Epithelial cells

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

APA (6^th Edition):

Agostini-Dreyer, Allyson M., 1. (2014). Role of endogenous IGFBP-3 in mammary epithelial cell apoptosis. (Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/43942/

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):

Agostini-Dreyer, Allyson M., 1986-. “Role of endogenous IGFBP-3 in mammary epithelial cell apoptosis.” 2014. Thesis, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/43942/.

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

MLA Handbook (7^th Edition):

Agostini-Dreyer, Allyson M., 1986-. “Role of endogenous IGFBP-3 in mammary epithelial cell apoptosis.” 2014. Web. 18 Jan 2021.

Vancouver:

Agostini-Dreyer, Allyson M. 1. Role of endogenous IGFBP-3 in mammary epithelial cell apoptosis. [Internet] [Thesis]. Rutgers University; 2014. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/43942/.

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

Council of Science Editors:

Agostini-Dreyer, Allyson M. 1. Role of endogenous IGFBP-3 in mammary epithelial cell apoptosis. [Thesis]. Rutgers University; 2014. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/43942/

Note: this citation may be lacking information needed for this citation format:
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Open Access Theses and Dissertations