The incidence of diabetes in the United States is increasing rapidly as a result of the obesity epidemic. Mouse models have increased our understanding of the pathogenesis of diabetes and other metabolic diseases. The projects described in this grant ufilize various genefic models to study the molecular mechanisms underiying energy homeostasis, and glucose and lipid metabolism. Core D provides accurate, timely and cost-effective phenotyping of mouse models generated by the Pis. Core D is directed by the PI of Project 3, Rex Ahima, who is also the director of the Penn Diabetes and Endocrinology Research Center (DERC) Mouse Phenotyping, Physiology and Metabolism Core. Core D supports the salary of a research specialist, supervised by the director Rex Ahima, to perform in vivo metabolic studies in mice. Core D uses state-of-the-art equipment and in vivo techniques. A Comprehensive Laboratory Animal Monitoring System (CLAMS) is used for assessment of food intake, drinking, energy expenditure, locomotor activity and sleep epochs. Nuclear Magnefic Resonance (NMR) and Dual Emission Xray Absorpfiometry (DEXA) are used for assessment of body composifion. Glucose homeostasis is evaluated with glucose and insulin tolerance tests, and insulin clamp and radioisotopic tracer kinetics. Core D also performs treadmill exercise, infrared thermography, blood pressure and heart rate monitoring, analysis of tissue chemistry, and tracer studies in isolated organs.

Public Health Relevance

Core D performs critical metabolic studies in mice generated by the Pis of this program, who lack the expertise or facilities to conduct these studies. Core D is directed by the PI of Project 3, Rex Ahima, and supporits the salary of a research specialist. The goal of Core D is to expedite the perfonnance of in vivo metabolic assays, ensure accuracy, and facilitate interactions among the Pis of the program project.

National Institute of Health (NIH)
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Research Program Projects (P01)
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Special Emphasis Panel (ZDK1-GRB-9)
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University of Pennsylvania
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Ahima, Rexford S (2016) Editorial: Unlocking Therapeutic Potential of Brown Fat. Mol Endocrinol 30:275-7
Iwafuchi-Doi, Makiko; Donahue, Greg; Kakumanu, Akshay et al. (2016) The Pioneer Transcription Factor FoxA Maintains an Accessible Nucleosome Configuration at Enhancers for Tissue-Specific Gene Activation. Mol Cell 62:79-91
Shearin, Abigail L; Monks, Bobby R; Seale, Patrick et al. (2016) Lack of AKT in adipocytes causes severe lipodystrophy. Mol Metab 5:472-9
Carr, Rotonya M; Ahima, Rexford S (2016) Pathophysiology of lipid droplet proteins in liver diseases. Exp Cell Res 340:187-92
Yang, Yizeng; Katz, Jonathan P (2016) KLF4 is downregulated but not mutated during human esophageal squamous cell carcinogenesis and has tumor stage-specific functions. Cancer Biol Ther 17:422-9
Jang, Cholsoon; Oh, Sungwhan F; Wada, Shogo et al. (2016) A branched-chain amino acid metabolite drives vascular fatty acid transport and causes insulin resistance. Nat Med 22:421-6
Jang, Jessica C; Chen, Gang; Wang, Spencer H et al. (2015) Macrophage-derived human resistin is induced in multiple helminth infections and promotes inflammatory monocytes and increased parasite burden. PLoS Pathog 11:e1004579
Soleimanpour, Scott A; Ferrari, Alana M; Raum, Jeffrey C et al. (2015) Diabetes Susceptibility Genes Pdx1 and Clec16a Function in a Pathway Regulating Mitophagy in β-Cells. Diabetes 64:3475-84
Park, Hyeong-Kyu; Ahima, Rexford S (2015) Physiology of leptin: energy homeostasis, neuroendocrine function and metabolism. Metabolism 64:24-34
Blanchet, Emilie; Van de Velde, Sam; Matsumura, Shigenobu et al. (2015) Feedback inhibition of CREB signaling promotes beta cell dysfunction in insulin resistance. Cell Rep 10:1149-57

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