肥胖小鼠的体重反弹会加速肝脂肪变性的发展，原因是脂肪组织功能受损。
Weight Regain in Formerly Obese Mice Hastens Development of Hepatic Steatosis Due to Impaired Adipose Tissue Function.
机构信息
Graduate Program in Immunology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
College of Literature Sciences and Arts, University of Michigan, Ann Arbor, Michigan, USA.
出版信息
Obesity (Silver Spring). 2020 Jun;28(6):1086-1097. doi: 10.1002/oby.22788. Epub 2020 Apr 13.
OBJECTIVE
Weight regain after weight loss is common, and there is evidence to suggest negative effects on health because of weight cycling. This study sought to investigate the impact of weight regain in formerly obese mice on adipose tissue architecture and stromal cell function.
METHODS
A diet-switch model was employed for obesity induction, weight loss, and weight regain in mice. Flow cytometry quantified adipose tissue leukocytes in adipose tissue. Liver and adipose tissue depots were compared to determine tissue-specific effects of weight cycling.
RESULTS
Epididymal white adipose tissue of formerly obese mice failed to expand in response to repeat exposure to high-fat diet and retained elevated numbers of macrophages and T cells. Weight regain was associated with disproportionally elevated liver mass, hepatic triglyceride content, serum insulin concentration, and serum transaminase concentration. These effects occurred despite an extended 6-month weight loss cycle and they demonstrate that formerly obese mice maintain durable alterations in their physiological response to weight regain. Conditioned media from epididymal adipose tissue of formerly obese mice inhibited adipogenesis of 3T3-L1 preadipocytes, suggesting a potential mechanism to explain failed epididymal adipose tissue expansion during weight regain.
CONCLUSIONS
Metabolic abnormalities related to defects in adipose tissue expansion and ongoing dysfunction manifest in formerly obese mice during weight regain.
目的
减肥后体重反弹很常见，有证据表明体重循环会对健康产生负面影响。本研究旨在探讨曾经肥胖的小鼠体重反弹对脂肪组织结构和基质细胞功能的影响。
方法
采用饮食转换模型诱导肥胖、减肥和体重反弹。流式细胞术定量分析脂肪组织中的白细胞。比较肝脏和脂肪组织库，以确定体重循环的组织特异性影响。
结果
曾经肥胖的小鼠的附睾白色脂肪组织在反复暴露于高脂肪饮食时无法扩张，并保留了升高的巨噬细胞和 T 细胞数量。体重反弹与肝质量不成比例升高、肝甘油三酯含量、血清胰岛素浓度和血清转氨酶浓度升高有关。尽管经历了长达 6 个月的减肥周期，但这些影响表明，曾经肥胖的小鼠仍然保持着对体重反弹的生理反应的持久改变。曾经肥胖的小鼠的附睾脂肪组织条件培养基抑制了 3T3-L1 前脂肪细胞的脂肪生成，这表明了一种可能的机制，可以解释体重反弹期间附睾脂肪组织扩张失败。
结论
在体重反弹期间，与脂肪组织扩张缺陷和持续功能障碍相关的代谢异常在曾经肥胖的小鼠中表现出来。
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