Diosgenin prevents high-fat diet-induced rat non-Alcoholic fatty liver disease through the AMPK and LXR signaling pathways

Abstract

non-alcoholic fatty liver disease (nafld) is a major public health concern worldwide. the aim of the present study was to observe the effect of diosgenin on nafld and investigatethe underlying mechanisms.diosgenin treatment increased the phosphorylation of amP-activated protein kinase (amPK) and acetyl-coa carboxylase (acc) in HepG2 cells. diosgenin signifcantly inhibited high glucose (HG)-induced triglyceride (tG) accumulation and sterol regulatory element-binding protein-1c (SreBP-1c) mrna increase in HepG2 cells, which were partially abolished by the amPK inhibitor compound c. Diosgenin also signifcantly inhibited the increase of liver X receptor (lXr) a mrna induced by HG or t0901317. However, t0901317-induced upregulation of lXra and SreBP-1c mrna was not blocked by compound c. following a high-fat diet for 16 weeks, the body and liver weights of the experimental rats were signifcantly increased, but this effect was signifcantly suppressed by diosgenin. Diosgenin and fenofbrate ameliorated lipid deposition in the liver and reduced the increase of hepatic TG content. Diosgenin signifcantly decreased the alanine aminotransferase (alt) level, whereas fenofibrate significantly increased the alt and aspartate aminotransferase levels. diosgenin also increased amPK and acc phosphorylation and suppressed lXra in the liver. in conclusion, the results of the present study suggested that diosgenin is a potential agent for preventing the development of nafld through the amPK and lXr signaling pathways.