Attenuation of high-fat diet-induced fatty liver through PPARα activation by stevioside. (June 2019)

• Record Type: Journal Article
• Authors: Jia, Chang-Hao; Zhang, Jun-Yan; Shen, Wei; Zhao, Xi; Xie, Mei-Lin
• Is Part Of: Journal of functional foods. Volume 57(2019)
• Page Start: 392
• Page End: 398
• Publication Date: 2019-06
• Subjects: Stevioside -- Fatty liver -- Peroxisome proliferator-activated receptor α; CPT-1A carnitine palmitoyltransferase-1A -- DGAT diacylglycerol acyltransferase -- FAS fatty acid synthase -- FFA free fatty acids -- PPARα peroxisome proliferator-activated receptor α -- SREBP-1c sterol regulatory element-binding protein-1c -- TC total cholesterol -- TG triglycerides; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2019.04.034
• Languages: English
• ISSNs: 1756-4646

Abstract

Graphical abstract: Highlights: Stevioside could attenuate the high-fat diet-induced fatty liver in rats. Stevioside could increase the hepatic PPARα and CPT-1A protein expressions. Stevioside could decrease the hepatic SREBP-1c, FAS and DGAT protein expressions. These effects of stevioside were reversed in the hepatocytes of PPARα gene silence. Abstract: This study aimed to investigate the effect of stevioside on fatty liver. Rats with hyperlipidemic fatty liver were treated with 75–150 mg/kg stevioside for 6 weeks. After oral administration of stevioside, the levels of serum and hepatic lipids and degree of hepatic steatosis were decreased. Stevioside treatment increased the expressions of hepatic peroxisome proliferator-activated receptor (PPAR)α and carnitine palmitoyltransferase-1A proteins and decreased the expressions of hepatic sterol regulatory element-binding protein-1c, fatty acid synthase and diacylglycerol acyltransferase proteins. Following treatment of oleic acid-stimulated hepatocytes with 100–400 μM stevioside, the intracellular lipids were also decreased. In the hepatocytes of PPARα gene silence, the lipid-lowering effect of stevioside was abolished, and its regulatory effects on PPARα-mediated target proteins were reversed. These findings demonstrated that stevioside was effective in treating fatty liver, and its mechanisms were associated with the increment of hepatic PPARα expression and subsequent modulation of its target gene expressions.