D Huang1, Z Zhang1, Z Dong2, R Liu1, J Huang1, G Xu3. 1. Department of Physiology, School of Medicine, Jinan University, 601 Huangpu Avenue West, Tianhe District, Guangzhou, 510632, Guangdong, China. 2. Department of Obesity and Metabolic Surgery, The First Affiliated Hospital of Jinan University, Guangzhou, China. 3. Department of Physiology, School of Medicine, Jinan University, 601 Huangpu Avenue West, Tianhe District, Guangzhou, 510632, Guangdong, China. xugeyangliang@163.com.
Abstract
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.
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.
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