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Friedline, Randall H.,Ko, Hwi Jin,Jung, Dae Young,Lee, Yongjin,Bortell, Rita,Dagdeviren, Sezin,Patel, Payal R.,Hu, Xiaodi,Inashima, Kunikazu,Kearns, Caitlyn,Tsitsilianos, Nicholas,Shafiq, Umber,Shultz The Federation of American Societies for Experimen 2016 The FASEB Journal Vol.30 No.3
<P>Obesity is characterized by a dysregulated immune system, which may causally associate with insulin resistance and type 2 diabetes. Despite widespread use of nonobese diabetic (NOD) mice, NOD with severe combined immunodeficiency (scid) mutation (SCID) mice, and SCID bearing a null mutation in the IL-2 common chain receptor (NSG) mice as animal models of human diseases including type 1 diabetes, the underlying metabolic effects of a genetically altered immune system are poorly understood. For this, we performed a comprehensive metabolic characterization of these mice fed chow or after 6 wk of a high-fat diet. We found that NOD mice had similar to 50% less fat mass and were 2-fold more insulin sensitive, as measured by hyperinsulinemic-euglycemic clamp, than C57BL/6 wild-type mice. SCID mice were also more insulin sensitive with increased muscle glucose metabolism and resistant to diet-induced obesity due to increased energy expenditure (similar to 10%) and physical activity (similar to 40%) as measured by metabolic cages. NSG mice were completely protected from diet-induced obesity and insulin resistance with significant increases in glucose metabolism in peripheral organs. Our findings demonstrate an important role of genetic background, lymphocytes, and cytokine signaling in diet-induced obesity and insulin resistance.</P>