Pectic Bee Pollen Polysaccharide from Rosa rugosa Alleviates Diet-Induced Hepatic Steatosis and Insulin Resistance via Induction of AMPK/mTOR-Mediated Autophagy.
Pectic Bee Pollen Polysaccharide from Rosa rugosa Alleviates Diet-Induced Hepatic Steatosis and Insulin Resistance via Induction of AMPK/mTOR-Mediated Autophagy.
复制标题
DOI:
10.3390/molecules22050699
复制
发表时间:
2017-04-28
期刊:
影响因子:
--
通讯作者:
Zhou Y
中科院分区:
文献类型:
--
作者:
Li X;Gong H;Yang S;Yang L;Fan Y;Zhou Y
Despite it is used as a nutraceutical against diabetes and obesity, the mechanism of action of bee pollen is still unclear. Pectic bee pollen polysaccharide (RBPP-P) was isolated from Rosa rugosa, and its structure was characterized by 13C-NMR and Fourier transform-infrared spectroscopy (FT-IR). Using high glucose and fatty acids-treated HepG2 cells and high fat diet (HFD)-induced obesity mice, we detected its effect on insulin function and lipid metabolism based on autophagy. RBPP-P contained arabinogalactan, rhamnogalacturonan I, and homogalacturonan domains. In vivo studies demonstrated that RBPP-P markedly ameliorated insulin resistance, glucose intolerance, and liver steatosis in obese mice. The suppressive effects of RBPP-P on liver steatosis and triglyceride content were mediated by increased autophagy and lipase expression in liver. In AMPK knockdown cells (prkaa 1/2−/− MEF) and HFD-fed mice tissues (liver, gonadal white adipose, and inguinal white adipose), RBPP-P enhanced autophagy in AMPK/mTOR-dependent way in liver, but not in adipose tissue. These findings demonstrated that bee pollen polysaccharide alleviated liver steatosis and insulin resistance by promoting autophagy via an AMPK/mTOR-mediated signaling pathway, suggesting that RBPP-P could be a novel therapeutic agent used for the treatment of obesity and diabetes.
登录
查看更多内容
影响因子:
1.4
作者:
Tu, Yan;Zhang, Guo-Feng;Diao, Qi-Yu
通讯作者:
Diao, Qi-Yu
影响因子:
11.2
作者:
Li F;Yuan Q;Rashid F
通讯作者:
Rashid F
影响因子:
21.3
作者:
通讯作者:
--
影响因子:
7
作者:
Coppack, SW
通讯作者:
Coppack, SW
影响因子:
4.9
作者:
Latorre, J.;Moreno-Navarrete, J. M.;Ortega, F. J.
通讯作者:
Ortega, F. J.