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Articles 1 - 4 of 4
Full-Text Articles in Endocrinology
Gpr75 Deficiency Attenuates High Fat Diet-Driven Obesity And Glucose Intolerance, Sakib Hossain
Gpr75 Deficiency Attenuates High Fat Diet-Driven Obesity And Glucose Intolerance, Sakib Hossain
NYMC Student Theses and Dissertations
Recently, a collaboration between Regeneron Pharmaceuticals and the Schwartzman-Garcia labs at New York Medical College published an exome sequencing study of individuals across the United Kingdom, United States, and Mexico which concluded that individuals possessing non-functioning, truncated mutations to the orphan g protein coupled receptor (GPCR), GPR75, had lower BMI and 54% reduced likelihood of obesity. The present study was undertaken to fully characterize the metabolic phenotype of Gpr75 deficient mice when fed a high fat diet (HFD) and explore potential mechanisms by which GPR75 activation links to increased adiposity and decreased glucose tolerance. After 14 weeks of HFD-feeding we …
Genetic And Cellular Models For The Study Of Ptk2b And Adam10 In Adaptive Thermogenesis And Metabolism, Jared S. Farrar
Genetic And Cellular Models For The Study Of Ptk2b And Adam10 In Adaptive Thermogenesis And Metabolism, Jared S. Farrar
Theses and Dissertations
In a cellular model, we demonstrate that the non-receptor protein tyrosine kinase 2 beta (PTK2B) plays a critical role in mouse cultured beige adipocyte differentiation. CRISPR/Cas9-mediated knock-out of Ptk2b results in non-differentiating white adipocytes and differentiated beige adipocytes with significantly reduced thermogenic gene and protein expression, enlarged lipid droplet size, and altered mitochondrial respiration. Together, these data in a cell culture system provide evidence for a role of PTK2B in the differentiation of mouse beige adipocytes.
In the process of developing a new mouse model utilizing the adipocyte selective Adipoq-Cre transgenic mouse, strong genetic linkage between a gene …
Metabolic Flexibility Among Women After A Single High Fat Meal, Alyssa Olenick
Metabolic Flexibility Among Women After A Single High Fat Meal, Alyssa Olenick
Masters Theses & Specialist Projects
PURPOSE: Obese women have increased rates of metabolic diseases compared to those of healthy weight status. Additionally, African-American (AA) women have higher rates of metabolic disease compared to Caucasian (CA) women. Metabolic inflexibility is the inability to adjust substrate oxidation in response to dietary intake; potentially leading to weight gain and the development of metabolic disease. Few studies have investigated the impact of weight status and/or ethnicity on the metabolic response of women to a single high fat meal. An acute unfavorable metabolic response may contribute to the higher incidence of metabolic disease among not only obese, but also AA …
Estrogen Receptor–Α In Medial Amygdala Neurons Regulates Body Weight, Pingwen Xu, Xuehong Cao, Yanlin He, Liangru Zhu, Yongjie Yang, Kenji Saito, Chunmei Wang, Xiaofeng Yan, Antentor Othrell Hinton Jr., Fang Zou, Hongfang Ding, Yan Xia, Chunling Yan, Gang Shu, San-Pin Wu, Bin Yang, Benjamin Feng, Deborah J. Clegg, Richard Demarchi, Sohaib A. Khan, Sophia Y. Tsai, Francesco J. Demayo, Qi Wu, Qingchun Tong, Yong Xu
Estrogen Receptor–Α In Medial Amygdala Neurons Regulates Body Weight, Pingwen Xu, Xuehong Cao, Yanlin He, Liangru Zhu, Yongjie Yang, Kenji Saito, Chunmei Wang, Xiaofeng Yan, Antentor Othrell Hinton Jr., Fang Zou, Hongfang Ding, Yan Xia, Chunling Yan, Gang Shu, San-Pin Wu, Bin Yang, Benjamin Feng, Deborah J. Clegg, Richard Demarchi, Sohaib A. Khan, Sophia Y. Tsai, Francesco J. Demayo, Qi Wu, Qingchun Tong, Yong Xu
Peer Reviewed Articles
Estrogen receptor–α (ERα) activity in the brain prevents obesity in both males and females. However, the ERα-expressing neural populations that regulate body weight remain to be fully elucidated. Here we showed that single-minded–1 (SIM1) neurons in the medial amygdala (MeA) express abundant levels of ERα. Specific deletion of the gene encoding ERα (Esr1) from SIM1 neurons, which are mostly within the MeA, caused hypoactivity and obesity in both male and female mice fed with regular chow, increased susceptibility to diet-induced obesity (DIO) in males but not in females, and blunted the body weight–lowering effects of a glucagon-like peptide-1–estrogen …