The Animal Metabolic Physiology Core is designed to meet the needs for characterization of rodent models that have alterations in glucose homeostasis, insulin action, leptin action and/or body composition. Its main function is to teach and provide consultation on ex vivo and in vivo methods to investigate the mechanisms for metabolic alterations in genetically-manipulated mouse models and in dietary models of obesity/leanness or insulin resistance/sensitivity. The specific objectives of the Core are 1) to teach and 2) to provide consultation to investigators in designing, carrying out and interpreting in vitro and in vivo studies to investigate the action of insulin and hormones that regulate energy balance such as leptin;glucose homeostasis;lipid metabolism;and body composition;3) The Core also performs a limited number of these studies on selected mouse or rat models created by or obtained by members of the Center. Services of the Core include ex vivo methods such as adipocyte isolation, and dissection and incubation of isolated skeletal muscles to study glucose transport, insulin signaling, leptin signaling, and glucose and fatty acid metabolism. In vivo methods assessing insulin action and glucose homeostasis include insulin tolerance test, glucose tolerance test, signaling assays in response to insulin injection or infusion, and measurement of glucose turnover, endogenous glucose production and glucose uptake by individual tissues during clamp studies. In vivo methods to investigate biological actions of orexigenic and anorexigenic hormones include measurement of food intake, energy expenditure and leptin signaling in peripheral tissues and hypothalamic nuclei. The Core also provides specialized equipment such as a DEXA scanner for non-invasive analysis of body composition and bone mineral density and a Coulter Counter for determining adipocyte number and size distribution. The Core Director, Barbara B. Kahn, MD, the Associate Core Director, Odile Peroni, PhD and the Research Associates who work with the Core have extensive experience with the metabolic and signaling assays offered by the Core. They are developing new assays to characterize additional aspects of integrated fuel metabolism and enerov homeostasis.

Public Health Relevance

The study of genetically engineered mouse models is an important tool to understand the physiology of newly discovered molecules. The Animal Metabolic Physiology Core is designed to meet the needs for characterization of rodent models that have alterations in glucose homeostasis, insulin action, leptin action and/or body composition. The Core provides both new and established investigators with the tools that will lead to important contributions to diabetes and obesity research.

National Institute of Health (NIH)
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Center Core Grants (P30)
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Special Emphasis Panel (ZDK1-GRB-2)
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Massachusetts General Hospital
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Krashes, Michael J; Shah, Bhavik P; Madara, Joseph C et al. (2014) An excitatory paraventricular nucleus to AgRP neuron circuit that drives hunger. Nature 507:238-42
Nomura, Naohiro; Nunes, Paula; Bouley, Richard et al. (2014) High-throughput chemical screening identifies AG-490 as a stimulator of aquaporin 2 membrane expression and urine concentration. Am J Physiol Cell Physiol 307:C597-605
Lee, Seung-Hwan; Huang, Hu; Choi, Kangduk et al. (2014) ROCK1 isoform-specific deletion reveals a role for diet-induced insulin resistance. Am J Physiol Endocrinol Metab 306:E332-43
Yuen, Grace J; Ausubel, Frederick M (2014) Enterococcus infection biology: lessons from invertebrate host models. J Microbiol 52:200-10
Chiappini, Franck; Catalano, Karyn J; Lee, Jennifer et al. (2014) Ventromedial hypothalamus-specific Ptpn1 deletion exacerbates diet-induced obesity in female mice. J Clin Invest 124:3781-92
Cohen, Paul; Levy, Julia D; Zhang, Yingying et al. (2014) Ablation of PRDM16 and beige adipose causes metabolic dysfunction and a subcutaneous to visceral fat switch. Cell 156:304-16
Wei, Nancy; Pan, Jessica; Pop-Busui, Rodica et al. (2014) Altered sphingoid base profiles in type 1 compared to type 2 diabetes. Lipids Health Dis 13:161
Kraus, Daniel; Yang, Qin; Kong, Dong et al. (2014) Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature 508:258-62
Oshiro, Noriko; Rapley, Joseph; Avruch, Joseph (2014) Amino acids activate mammalian target of rapamycin (mTOR) complex 1 without changing Rag GTPase guanyl nucleotide charging. J Biol Chem 289:2658-74
Ruan, Ye Chun; Wang, Yan; Da Silva, Nicolas et al. (2014) CFTR interacts with ZO-1 to regulate tight junction assembly and epithelial differentiation through the ZONAB pathway. J Cell Sci 127:4396-408

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