Tian Dongmei, Zhong Xiaoyan, Fu Liya, Zhu Wanlong, Liu Xin, Wu Zhigui, Li Yue, Li Xue, Li Xuesen, Tao Xuemei, Wei Qiming, Yang Xuping, Huang Yilan
Department of Pharmacy, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China; School of Pharmacy, Southwest Medical University, Luzhou 646000, China.
Department of Pharmacy, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.
Phytomedicine. 2022 May;99:154031. doi: 10.1016/j.phymed.2022.154031. Epub 2022 Mar 4.
Recent studies have shown that polysaccharides from Anoectochilus roxburghii (Wall.) Lindl. (ARPs) can reduce blood glucose levels, ameliorate oxidative stress and inflammation. However, whether ARPs have a beneficial effect on diet-induced obesity remain to be determined.
This study aims to investigate the effect and mechanism of ARPs in improving obesity and metabolic disorders induced by high-fat diet (HFD).
In this study, 6-week-old male mice were fed with HFD or chow diet for 13 weeks, and a dietary supplementation with ARPs was carried out. Glucose tolerance test and insulin tolerance test were performed to measure the glucose tolerance and insulin sensitivity. Adipose tissue and liver were isolated for analysis by qRT-PCR, Western blotting, hematoxylin-eosin staining and immunostaining.
At week 13, body weight and fat mass were significantly increased by HFD, but ARPs supplementation abolished these phenotypes. Compared with HFD group, thermogenic genes including Ucp-1, Pgc-1α, Prdm16 and Dio2 in adipose tissue were up-regulated in ARPs-treated mice. In addition, ARPs decreased liver lipid accumulation by reducing lipid synthesis and increasing oxidation. Meanwhile, dyslipidemia and insulin resistance induced by HFD were improved by ARPs. Mechanistically, ARPs can promote fat thermogenesis via AMPK/SIRT1/PGC-1α signaling pathway.
Dietary supplementation of ARPs can protect mice against diet-induced obesity, fatty liver and insulin resistance. Our study reveals a potential therapeutic effect for ARPs in regulating energy homeostasis.
最近的研究表明,金线莲多糖(ARPs)可以降低血糖水平,改善氧化应激和炎症。然而,ARPs对饮食诱导的肥胖是否具有有益作用仍有待确定。
本研究旨在探讨ARPs改善高脂饮食(HFD)诱导的肥胖和代谢紊乱的作用及机制。
在本研究中,6周龄雄性小鼠喂食HFD或普通饮食13周,并进行ARPs饮食补充。进行葡萄糖耐量试验和胰岛素耐量试验以测量葡萄糖耐量和胰岛素敏感性。分离脂肪组织和肝脏,通过qRT-PCR、蛋白质免疫印迹、苏木精-伊红染色和免疫染色进行分析。
在第13周时,HFD显著增加了体重和脂肪量,但补充ARPs消除了这些表型。与HFD组相比,ARPs处理的小鼠脂肪组织中包括Ucp-1、Pgc-1α、Prdm16和Dio2在内的产热基因上调。此外,ARPs通过减少脂质合成和增加氧化来降低肝脏脂质积累。同时,ARPs改善了HFD诱导的血脂异常和胰岛素抵抗。机制上,ARPs可通过AMPK/SIRT1/PGC-1α信号通路促进脂肪产热。
饮食补充ARPs可以保护小鼠免受饮食诱导的肥胖、脂肪肝和胰岛素抵抗。我们的研究揭示了ARPs在调节能量稳态方面的潜在治疗作用。