Abstract
Non-alcoholic steatosis and insulin resistance are critical health problems and cause metabolic complications worldwide. In this study, we investigated the molecular mechanism of Polygonum multiflorum Thunb. (PM) against hepatic lipid accumulation and insulin resistance by using in vitro and in vivo models. PM extract significantly attenuated the accumulation of lipid droplets and hepatic triglyceride in free fatty acid (FFA)-exposed HepG2 cells. PM extract increased the AMPK and ACC phosphorylation and GLUT4 expression, whose levels were downregulated in FFA-exposed cells. PM extract also decreased precursor and mature forms of SREBP-1 in FFA-exposed cells. C57BL/6 mice fed with normal diet (ND) or high-fat diet (HFD) were administered PM extract (100 mg/kg) or vehicle orally for 16 weeks. PM extract attenuated the increases of the epididymal and perirenal fats on HFD feeding. PM extract markedly reduced hepatic lipid accumulation and fasting glucose levels, and improved glucose and insulin sensitivity in HFD-fed mice. HFD-fed mice decreased the AMPK and ACC phosphorylation and GLUT4 expression, and increased precursor and mature forms of SREBP-1; these changes were significantly restored by PM extract. In conclusion, PM extract alleviates non-alcoholic steatosis and insulin resistance through modulating the expression of proteins on lipid metabolism and glucose transport in the liver.
Highlights
Non-alcoholic fatty liver disease (NAFLD) encompasses from simple steatosis to nonalcoholic steatohepatitis (NASH), advanced fibrosis or cirrhosis and hepatocellular carcinoma, and is a rising health concern linked to the development of numerous health problems and high costs
Due to the effect of Polygonum multiflorum Thunb. (PM) on limiting lipid accumulation, we further investigated whether PM extract affects the expression of proteins regulating lipolysis (AMPK and acetyl-CoA carboxylase (ACC)) and lipogenesis (SREBP), as well as GLUT 4 in HepG2 cells
We investigated the therapeutic effect of PM and its molecular mechanisms on the development
Summary
Non-alcoholic fatty liver disease (NAFLD) encompasses from simple steatosis to nonalcoholic steatohepatitis (NASH), advanced fibrosis or cirrhosis and hepatocellular carcinoma, and is a rising health concern linked to the development of numerous health problems and high costs. The incidence of NAFLD is higher in people with type 2 diabetes (60–70%), and in those who are obese or morbidly obese (75–92%), compared to the general population [4]. The non-alcoholic fatty liver (simple steatosis), the early stage of NAFLD, is accompanied by excessive lipid or triglyceride (TG) deposition in hepatocyte without significant alcohol intake or the initiation of inflammation. Non-alcoholic steatosis is considered to be an optimal therapeutic stage of NAFLD since it is reversible to normal condition by restoring the metabolic homeostasis
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