Melon GliSODin® Prevents Diet-Induced NASH Onset by Reducing Fat Synthesis and Improving Liver Function.

Nakamura Nakamura,Kitamura Kitamura,Uchida Uchida,Yokoyama Yokoyama,Kumadaki Kumadaki,Watanabe Watanabe,Tsubota Tsubota

doi:10.3390/nu11081779

Abstract

A high-calorie diet causes fat accumulation and oxidative stress in the liver, leading to fatty liver and eventually non-alcoholic steatohepatitis (NASH). Melon GliSODin® is used as a nutritional supplement because of its antioxidant activity. This study aimed to assess the antioxidant activity of Melon GliSODin® and its effectiveness in preventing NASH, which primarily results from oxidative stress. Furthermore, we verified the protective effect of Melon GliSODin® by administering it to a mouse model of diet-induced NASH. Melon GliSODin® suppressed liver fibrosis and fat accumulation, which is characteristic of the NASH phenotype. Gene expression analysis confirmed the suppression of fat synthesis and activation of antioxidative mechanisms. These results show that Melon GliSODin® mitigates NASH onset at the molecular level, suggesting its potential application as a NASH preventive agent.

Highlights

Antioxidants quench reactive oxygen species [1]; their levels decrease with age, causing a corresponding increase in oxidative stress [2,3,4]
Liver hypertrophy was clearly suppressed in the Melon GliSODin® -administered group rather than in the high-cholesterol diet (HC) group, as indicated by both liver weights and via visual inspection of the organs, as shown in post-dissection photographs (Figure 1D,E)
We analyzed lipid parameters in plasma samples harvested during euthanasia and the results show that total cholesterol in the Melon GliSODin® (MEL) group decreased significantly and other parameters tended to decline (Figure 1F–I) relative to the HC group

Summary

Introduction

Antioxidants quench reactive oxygen species [1]; their levels decrease with age, causing a corresponding increase in oxidative stress [2,3,4]. Oxidation leads to the production of free radicals leading to chain reactions potentially causing damage to living organisms. It is, becoming progressively more important to consume antioxidants with food or as dietary supplements. Accumulation of oxidative stress is considered to contribute to the development of obesity and other lifestyle-related diseases [5]. Non-alcoholic fatty liver disease (NAFLD) usually occurs in individuals with obesity and insulin resistance [6], but not in those with alcoholic liver injury.

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