Succinate Enhances Lipolysis and Decreases Adipocytes Size in Both Subcutaneous and Visceral Adipose Tissue from High-Fat-Diet-Fed Obese Mice

琥珀酸可增强高脂饮食肥胖小鼠的脂肪分解并减少皮下和内脏脂肪组织中的脂肪细胞大小

阅读:9
作者:Tengteng Ji, Bing Fang, Ming Zhang, Yaqiong Liu

Abstract

Obesity is a risk factor for many chronic diseases related to the overexpansion of adipose tissue during obesity, leading to metabolic dysfunction and ectopic lipids. Previous studies reported a close relationship between succinate and obesity and its co-morbidities, and studies have also reported on its anti-obesity potential. To confirm its efficacy in obesity interventions, we supplemented mice with obesity induced by a high-fat diet with succinate (1.5% m/v in drinking water) for 11 weeks without changing the diet. After succinate supplementation, the changes in body weight, adipose tissue deposition, glucose tolerance, energy expenditure and lipid metabolism were evaluated. It was found that succinate supplementation significantly decreased subcutaneous adipose tissue (HFD: 4239.3 ± 211.2 mg; HFD-SA: 3268.9 ± 265.7 mg. p < 0.05), triglyceride contents (decreased by 1.53 mmol/g and 0.39 mmol/g in eWAT and ingWAT, respectively, p < 0.05) and NEFA (decreased by 1.41 μmol/g and 1.31 μmol/g in eWAT and ingWAT, respectively, p < 0.05). The adipocytes' sizes all significantly decreased in both subcutaneous and visceral adipose tissue (the proportion of adipocytes with diameters larger than 100 μm in eWAT and ingWAT decreased by 16.83% and 11.96%, respectively. p < 0.05). Succinate significantly enhanced lipolysis in adipose tissue (eWAT: Adrb3, Hsl and Plin1; ingWAT: Hsl and CPT1a; p < 0.05), whereas the expression of lipogenesis-related genes remained unchanged (p > 0.05). Succinate supplementation also enhanced the activity of BAT by stimulating the expression of Ucp1 and Cidea (p < 0.05). Our results reported that succinate has a potential beneficial effect on obesity pathogenesis but cannot efficiently decrease bodyweight.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。