Suppr超能文献

壳聚糖补充剂通过激活单磷酸腺苷(AMP)激活的蛋白激酶和抑制脂肪生成相关基因来减轻高脂饮食增强的大鼠脂肪生成。

Supplementation of chitosan alleviates high-fat diet-enhanced lipogenesis in rats via adenosine monophosphate (AMP)-activated protein kinase activation and inhibition of lipogenesis-associated genes.

作者信息

Chiu Chen-Yuan, Chan Im-Lam, Yang Tsung-Han, Liu Shing-Hwa, Chiang Meng-Tsan

机构信息

†Institute of Toxicology, College of Medicine, National Taiwan University, Taipei 100, Taiwan.

‡Department of Food Science, College of Life Science, National Taiwan Ocean University, Keelung 202, Taiwan.

出版信息

J Agric Food Chem. 2015 Mar 25;63(11):2979-88. doi: 10.1021/acs.jafc.5b00198. Epub 2015 Mar 16.

Abstract

This study investigated the role of chitosan in lipogenesis in high-fat diet-induced obese rats. The lipogenesis-associated genes and their upstream regulatory proteins were explored. Diet supplementation of chitosan efficiently decreased the increased weights in body, livers, and adipose tissues in high-fat diet-fed rats. Chitosan supplementation significantly raised the lipolysis rate; attenuated the adipocyte hypertrophy, triglyceride accumulation, and lipoprotein lipase activity in epididymal adipose tissues; and decreased hepatic enzyme activities of lipid biosynthesis. Chitosan supplementation significantly activated adenosine monophosphate (AMP)-activated protein kinase (AMPK) phosphorylation and attenuated high-fat diet-induced protein expressions of lipogenic transcription factors (PPAR-γ and SREBP1c) in livers and adipose tissues. Moreover, chitosan supplementation significantly inhibited the expressions of downstream lipogenic genes (FAS, HMGCR, FATP1, and FABP4) in livers and adipose tissues of high-fat diet-fed rats. These results demonstrate for the first time that chitosan supplementation alleviates high-fat diet-enhanced lipogenesis in rats via AMPK activation and lipogenesis-associated gene inhibition.

摘要

本研究调查了壳聚糖在高脂饮食诱导的肥胖大鼠脂肪生成中的作用。探索了与脂肪生成相关的基因及其上游调节蛋白。在高脂饮食喂养的大鼠中,饮食补充壳聚糖有效地降低了体重、肝脏和脂肪组织重量的增加。补充壳聚糖显著提高了脂肪分解率;减轻了附睾脂肪组织中的脂肪细胞肥大、甘油三酯积累和脂蛋白脂肪酶活性;并降低了肝脏脂质生物合成的酶活性。补充壳聚糖显著激活了单磷酸腺苷(AMP)激活的蛋白激酶(AMPK)磷酸化,并减弱了高脂饮食诱导的肝脏和脂肪组织中脂肪生成转录因子(PPAR-γ和SREBP1c)的蛋白表达。此外,补充壳聚糖显著抑制了高脂饮食喂养大鼠肝脏和脂肪组织中下游脂肪生成基因(FAS、HMGCR、FATP1和FABP4)的表达。这些结果首次证明,补充壳聚糖通过激活AMPK和抑制脂肪生成相关基因来减轻高脂饮食增强的大鼠脂肪生成。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验