ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2016
Genetic ablation of lymphocytes and cytokine signaling in nonobese diabetic mice prevents diet-induced obesity and insulin resistance.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- T cell knockout attenuates HFD-induced increases in blood pressure in female and male Dahl rats.Clinical science (London, England : 1979) · 2025Article
- Hyperlipidemia drives tumor growth in a mouse model of obesity-accelerated breast cancer growth.Cancer & metabolism · 2025Article
- Article
- The role of obesity and bariatric surgery-induced weight loss in breast cancer.Cancer metastasis reviews · 2022Review
- Article
- The Role of the Adipokine Leptin in Immune Cell Function in Health and Disease.Frontiers in immunology · 2020Review
- CD4Frontiers in immunology · 2020Article
- Tipping the scales: Are females more at risk for obesity- and high-fat diet-induced hypertension and vascular dysfunction?British journal of pharmacology · 2019Review
- Insights from engraftable immunodeficient mouse models of hyperinsulinaemia.Scientific reports · 2017Article
- Oral Corticosterone Administration Reduces Insulitis but Promotes Insulin Resistance and Hyperglycemia in Male Nonobese Diabetic Mice.The American journal of pathology · 2017Article
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
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 γ 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.
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Registered trials
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