Abstract

The aim of this study was to evaluate the long-term effects of grape pomace ethanol extract (GPE) with or without omija fruit ethanol extract (OFE) on adiposity, hepatic steatosis, and inflammation in diet-induced obese mice. Male C57BL/6J mice were fed a high-fat diet (HFD) as the control diet and HFD plus GPE (0.5%, w/w) with or without OFE (0.05%, w/w) as the experimental diet for 12 weeks. GPE alone did not significantly affect adipogenesis and hepatic steatosis. However, the supplementation of GPE + OFE significantly lowered body weight gain, white adipose tissue weight, adipocyte size, and plasma free fatty acid and adipokines (leptin, PAI-1, IL-6, and MCP-1) levels in HFD-fed mice compared to those of the control group. These beneficial effects of GPE + OFE were partly related to the decreased expression of lipogenic and inflammatory genes in white adipose tissue. GPE + OFE supplementation also significantly lowered liver weight and ameliorated fatty liver by inhibiting expression of hepatic genes involved in fatty acid and cholesterol syntheses as well as inflammation and by activating hepatic fatty acid oxidation. These findings suggest that the combined ethanol extract of grape pomace and omija fruit has the potential to improve adiposity and fatty liver in diet-induced obese mice.

Highlights

  • Obesity, a metabolic disease characterized by an excessive accumulation of fat in white adipose tissue (WAT), is associated with chronic inflammation and is considered a risk factor of nonalcoholic fatty liver disease (NAFLD)

  • Mice supplemented with grape pomace ethanol extract (GPE) + omija fruit ethanol extract (OFE) showed a significantly lower body weight gain compared to the high-fat diet (HFD) control (Figure 1(a))

  • We demonstrated that the combination of GPE and OFE led to a favorable effect on adiposity, hepatic steatosis, and inflammation in HFD-induced obese mice, GPE alone did not significantly decrease body weight, body fat, and hepatic lipid accumulation

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Summary

Introduction

A metabolic disease characterized by an excessive accumulation of fat in white adipose tissue (WAT), is associated with chronic inflammation and is considered a risk factor of nonalcoholic fatty liver disease (NAFLD). WAT secretes various inflammation-related adipocytokines, and the dysregulated production of adipocytokines promotes NAFLD. Visceral WAT is directly linked to the severity of hepatic inflammation and fibrosis in NAFLD, independent of hepatic steatosis [1]. Visceral WAT might promote NAFLD by the release of free fatty acids that are delivered directly into the portal vein [2]. There is a close relationship between visceral and liver fat contents in obese and nonobese individuals [3,4,5]. Lipogenesis is an important metabolic pathway regulating adipose and hepatic fat accumulation [6]

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