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- Title
Genetic ablation of lymphocytes and cytokine signaling in nonobese diabetic mice prevents diet-induced obesity and insulin resistance.
- Authors
Friedline, Randall H.; Hwi Jin Ko; Dae Young Jung; Yongjin Lee; Bortell, Rita; Dagdeviren, Sezin; Patel, Payal R.; Xiaodi Hu; Kunikazu Inashima; Caitlyn Kearns; Tsitsilianos, Nicholas; Shafiq, Umber; Shultz, Leonard D.; Ki Won Lee; Greiner, Dale L.; Kim, Jason K.
- Abstract
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 ~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 (~10%) and physical activity (~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.
- Subjects
LYMPHOCYTES; CYTOKINES; CELLULAR signal transduction; PEOPLE with diabetes; LABORATORY mice; OBESITY; INSULIN resistance
- Publication
FASEB Journal, 2016, Vol 30, Issue 3, p1328
- ISSN
0892-6638
- Publication type
Article
- DOI
10.1096/fj.15-280610