Lack of mature lymphocytes results in obese but metabolically healthy mice when fed a high-fat diet.

摘要: Obesity is characterized by chronic inflammation and immune dysregulation, as well insulin resistance, but the link between obesity adaptive immunity remains to be fully studied. To elucidate role of on body composition, glucose homeostasis inflammation, recombination-activating gene 1 knockout (Rag1−/−) mice, without mature T-lymphocytes or B-lymphocytes, were maintained a low- high-fat diet (LFD HFD, respectively) for 11 weeks. Rag1−/− mice fed HFD gained significantly more weight had increased fat compared with wild type. Downregulation energy expenditure brown uncoupling protein UCP-1 UCP-3 expression noticed in HFD-fed LFD. decreased intake LFD consistent agouti-related pro-opiomelanocortin levels hypothalamus. Moreover, type, lower interleukin (IL)-4 levels, cytokine recently found induce browning white adipocytes, higher IL-12 mice. Despite that obese, they similar glucose, adiponectin while leptin was marginally increased. Mice deficiency are partly owing expenditure, metabolically normal, suggesting lymphocytes have necessary roles development obesity-related metabolic dysregulation.