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Anti-Obesity Effects of Aster spathulifolius Extract in High-Fat Diet-Induced Obese Rats

机译:紫菀提取物对高脂饮食诱导肥胖大鼠的抗肥胖作用

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The aim of this study was to investigate the anti-obesity and antihyperlipidemic efficacy and molecular mechanisms of Aster spathulifolius Maxim extract (ASE) in rats with high-fat diet (HFD)-induced obesity. Rats were separately fed a normal diet or a HFD for 8 weeks, then they were treated with ASE (62.5, 125, or 250mg/kg) for another 4.5 weeks. The ASE supplementation significantly lowered body weight gain, visceral fat pad weights, serum lipid levels, as well as hepatic lipid levels in HFD-induced obese rats. Histological analysis showed that the ASE-treated group showed lowered numbers of lipid droplets and smaller size of adipocytes compared to the HFD group. To understand the mechanism of action of ASE, the expression of genes and proteins involved in obesity were measured in liver and skeletal muscle. The expression of fatty acid oxidation and thermogenesis-related genes (e.g., PPAR-, ACO, CPT1, UCP2, and UCP3) of HFD-induced obese rats were increased by ASE treatment. On the other hand, ASE treatment resulted in decreased expression of fat intake-related gene ACC2 and lipogenesis-related genes (e.g., SREBP-1c, ACC1, FAS, SCD1, GPATR, AGPAT, and DGAT). Furthermore, ASE treatment increased the level of phosphorylated AMPK in obese rats. Similarly, the level of phosphorylated ACC, a target protein of AMPK in ASE groups, was increased by ASE treatment compared with the HFD group. These results suggest that ASE attenuated visceral fat accumulation and improved hyperlipidemia in HFD-induced obese rats by increasing lipid metabolism through the regulation of AMPK activity and the expression of genes and proteins involved in lipolysis and lipogenesis.
机译:本研究旨在探讨紫菀提取物(ASE)对高脂饮食(HFD)诱导肥胖大鼠的抗肥胖和抗高血脂功效及分子机制。分别给大鼠喂食正常饮食或HFD8周,然后用ASE(62.5、125或250mg/kg)治疗4.5周。补充ASE可显著降低HFD诱导的肥胖大鼠的体重增加、内脏脂肪垫重量、血脂水平以及肝脂水平。组织学分析显示,与HFD组相比,ASE治疗组的脂滴数量减少,脂肪细胞尺寸更小。为了了解ASE的作用机制,测量了肝脏和骨骼肌中与肥胖有关的基因和蛋白质的表达。ASE处理可增加HFD诱导的肥胖大鼠脂肪酸氧化和产热相关基因(如PPAR-、ACO、CPT1、UCP2和UCP3)的表达。另一方面,ASE 治疗导致脂肪摄入相关基因 ACC2 和脂肪生成相关基因(例如 SREBP-1c、ACC1、FAS、SCD1、GPATR、AGPAT 和 DGAT)的表达降低。此外,ASE处理增加了肥胖大鼠磷酸化AMPK的水平。同样,与 HFD 组相比,ASE 组 AMPK 的靶蛋白磷酸化 ACC 水平通过 ASE 处理增加。这些结果表明,ASE通过调节AMPK活性以及参与脂肪分解和脂肪生成的基因和蛋白质的表达来增加脂质代谢,从而减轻HFD诱导的肥胖大鼠的内脏脂肪堆积并改善高脂血症。

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