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Dietary Silk Peptide Prevents High-Fat Diet-Induced Obesity and Promotes Adipose Browning by Activating AMP-Activated Protein Kinase in Mice

机译:膳食丝肽可防止高脂饮食诱导的肥胖,并通过激活小鼠中的AMP活化蛋白激酶促进脂肪褐变

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摘要

Obesity is associated with metabolic syndrome and other chronic diseases, and is caused when the energy intake is greater than the energy expenditure. We aimed to determine the mechanism whereby acid-hydrolyzed silk peptide (SP) prevents high-fat diet-induced obesity, and whether it induces browning and fatty acid oxidation (FAO) in white adipose tissue (WAT), using in vivo and ex vivo approaches. We determined the effects of dietary SP in high-fat diet-fed obese mice. The expression of adipose tissue-specific genes was quantified by western blotting, qRT-PCR, and immunofluorescence analysis. We also investigated whether SP directly induces browning in primarily subcutaneous WAT-derived adipocytes. Our findings demonstrate that SP has a browning effect in WAT by upregulating AMP-activated Protein Kinase (AMPK) phosphorylation and uncoupling protein 1 (UCP1) expression. SP also suppresses adipogenesis and promotes FAO, implying that it may have potential as an anti-obesity drug.
机译:肥胖与代谢综合征和其他慢性疾病有关,并且当能量摄入量大于能量消耗时导致。我们的目标是确定酸 - 水解丝肽(SP)的机制可防止高脂肪饮食诱导的肥胖症,以及它是否在白色脂肪组织(WAT)中诱导褐变和脂肪酸氧化(粮农组织),在体内和exvivo中使用方法。我们确定了膳食SP在高脂饮食喂养肥胖小鼠中的影响。通过蛋白质印迹,QRT-PCR和免疫荧光分析量化脂肪组织特异性基因的表达。我们还研究了SP是否直接诱导褐变,主要在皮下脱湿的脂肪细胞中。我们的研究结果表明,通过上调AMP活化的蛋白激酶(AMPK)磷酸化和解偶联蛋白1(UCP1)表达,SP在Wat具有褐色效果。 SP还抑制脂肪发生并促进粮农组织,这意味着它可能具有抗肥胖药物的潜力。

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