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蓬萊葛能通过激活 AMP 激活的蛋白激酶和调节脂质代谢来减轻饮食诱导的肥胖。

Boesenbergia pandurata attenuates diet-induced obesity by activating AMP-activated protein kinase and regulating lipid metabolism.

机构信息

Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, 50 Yonsei-ro, Seodaemun-gu, Seoul 120-749, Korea.

Department of Biomaterials Science and Engineering, Yonsei University, 50 Yonsei-ro, Seodaemun-gu, Seoul 120-749, Korea.

出版信息

Int J Mol Sci. 2012;13(1):994-1005. doi: 10.3390/ijms13010994. Epub 2012 Jan 17.

DOI:10.3390/ijms13010994
PMID:22312299
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3269733/
Abstract

Obesity, a chronic metabolic disorder, is characterized by enlarged fat mass and dysregulation of lipid metabolism. The medicinal plant, Boesenbergia pandurata (Roxb.) Schltr., has been reported to possess anti-oxidative and anti-inflammatory properties; however, its anti-obesity activity is unexplored. The present study was conducted to determine whether B. pandurata extract (BPE), prepared from its rhizome parts, attenuated high-fat diet (HFD)-induced obesity in C57BL/6J mice. The molecular mechanism was investigated in 3T3-L1 adipocytes and HepG2 human hepatoma cells. BPE treatment decreased triglyceride accumulation in both 3T3-L1 adipocytes and HepG2 hepatocytes by activating AMP-activated protein kinase (AMPK) signaling and regulating the expression of lipid metabolism-related proteins. In the animal model, oral administration of BPE (200 mg/kg/day for 8 weeks) significantly reduced HFD-induced body weight gain without altering the amount of food intake. In addition, elevated serum levels of total cholesterol, low-density lipoprotein cholesterol, and triglycerides were suppressed by BPE administration. Fat pad masses were reduced in BPE-treated mice, as evidenced by reduced adipocyte size. Furthermore, BPE protected against the development of nonalcoholic fatty liver by decreasing hepatic triglyceride accumulation. BPE also activated AMPK signaling and altered the expression of lipid metabolism-related proteins in white adipose tissue and liver. Taken together, these findings indicate that BPE attenuates HFD-induced obesity by activating AMPK and regulating lipid metabolism, suggesting a potent anti-obesity agent.

摘要

肥胖是一种慢性代谢紊乱,其特征为脂肪量增大和脂质代谢失调。药用植物蓬莪术(Roxb.)Schltr. 已被报道具有抗氧化和抗炎特性;然而,其抗肥胖活性尚未得到探索。本研究旨在确定蓬莪术根茎部分制备的提取物(BPE)是否能减轻 C57BL/6J 小鼠高脂饮食(HFD)诱导的肥胖。在 3T3-L1 脂肪细胞和 HepG2 人肝癌细胞中研究了其分子机制。BPE 处理通过激活 AMP 激活的蛋白激酶(AMPK)信号通路和调节脂质代谢相关蛋白的表达,减少了 3T3-L1 脂肪细胞和 HepG2 肝细胞中的甘油三酯积累。在动物模型中,BPE(200mg/kg/天,连续 8 周)的口服给药显著减少了 HFD 诱导的体重增加,而不改变食物摄入量。此外,BPE 给药可降低血清总胆固醇、低密度脂蛋白胆固醇和甘油三酯的水平。BPE 处理的小鼠脂肪垫质量减少,这表明脂肪细胞大小减小。此外,BPE 通过减少肝内甘油三酯积累来预防非酒精性脂肪肝的发展。BPE 还通过激活 AMPK 信号通路和改变白色脂肪组织和肝脏中脂质代谢相关蛋白的表达来发挥作用。综上所述,这些发现表明 BPE 通过激活 AMPK 和调节脂质代谢来减轻 HFD 诱导的肥胖,提示其为一种有效的抗肥胖剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abed/3269733/5ac4b2232f7d/ijms-13-00994f4.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abed/3269733/ef67403b94ec/ijms-13-00994f2.jpg
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