Purpose

Caloric restriction (CR) and Roux-en-Y Gastric Bypass (RYGB) are considered effective means of body weight control, but the mechanism by which CR and RYGB protect against high-fat diet (HFD)-induced obesity remains elusive. The browning of white adipose tissue (WAT) is a potential approach to combat obesity. Here we assess whether browning of WAT is involved in CR- and RYGB-treatment.

Methods

The average size of adipocytes was determined by histological analysis. Expression of thermogenic genes in both human subjects and mice were measured by quantitative real-time PCR and immunohistochemical staining.

Results

The average size of adipocytes was bigger, while the expression of thermogenic genes such as uncoupling protein 1 (UCP1), nuclear factor erythroid-2 like 1 (NRF1) and PPARγ coactivator-1 α (PGC1α) were lower in the WAT of obese subjects when compared to lean controls. Both CR and RYGB promoted weight and fat loss. Increment of the average adipocytes size and down-regulation of thermogenic genes were significantly reversed by both CR and RYGB in the WAT of obese mice.

Conclusions

Our findings showed that CR and RYGB significantly improved high-fat diet-induced lipid accumulation by promoting the browning of WAT.

中文翻译：

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热量限制和 Roux-en-Y 胃旁路术促进小鼠白色脂肪组织褐变

目的

热量限制 (CR) 和 Roux-en-Y 胃旁路术 (RYGB) 被认为是控制体重的有效手段，但 CR 和 RYGB 防止高脂饮食 (HFD) 引起的肥胖的机制仍然难以捉摸。白色脂肪组织 (WAT) 的褐变是对抗肥胖的一种潜在方法。在这里，我们评估 WAT 的褐变是否与 CR 和 RYGB 处理有关。

方法

通过组织学分析确定脂肪细胞的平均大小。通过定量实时 PCR 和免疫组织化学染色测量人类受试者和小鼠中产热基因的表达。

结果

脂肪细胞的平均大小较大，而在肥胖受试者的WAT中，解偶联蛋白1（UCP1）、核因子红细胞2样1（NRF1）和PPARγ辅激活因子1α（PGC1α ）等产热基因的表达较低与精益控制相比。CR 和 RYGB 都促进了体重和脂肪的减少。在肥胖小鼠的 WAT 中，CR 和 RYGB 均显着逆转了平均脂肪细胞大小的增加和产热基因的下调。

结论

我们的研究结果表明，CR 和 RYGB 通过促进 WAT 褐变显着改善高脂饮食诱导的脂质积累。