Uric acid and transforming growth factor in fructose-induced production of reactive oxygen species in skeletal muscle

被引：32

作者：

Madlala, Hlengiwe P. ^{[1
]}

Maarman, Gerald J. ^{[1
]}

Ojuka, Edward ^{[1
]}

机构：

[1] Univ Cape Town, Dept Human Biol, Exercise Sci & Sports Med Unit, ZA-7925 Cape Town, Western Cape, South Africa

来源：

NUTRITION REVIEWS | 2016年 / 74卷 / 04期

基金：

新加坡国家研究基金会;

关键词：

fructose; mitochondrial dysfunction; reactive oxygen species; transforming growth factor; uric acid; NADPH OXIDASE ACTIVATION; DE-NOVO LIPOGENESIS; OXIDATIVE STRESS; INSULIN-RESISTANCE; MITOCHONDRIAL DYSFUNCTION; XANTHINE-OXIDASE; CARDIOVASCULAR-DISEASE; NITRIC-OXIDE; CORN SYRUP; VASCULAR DYSFUNCTION;

D O I：

10.1093/nutrit/nuv111

中图分类号：

R15 [营养卫生、食品卫生]; TS201 [基础科学];

学科分类号：

100403 ;

摘要：

The consumption of fructose, a major constituent of the modern diet, has raised increasing concern about the effects of fructose on health. Research suggests that excessive intake of fructose (> 50 g/d) causes hyperuricemia, insulin resistance, mitochondrial dysfunction, de novo lipogenesis by the liver, and increased production of reactive oxygen species (ROS) in muscle. In a number of tissues, uric acid has been shown to stimulate the production of ROS via activation of transforming growth factor beta 1 and NADPH (nicotinamide adenine dinucleotide phosphate) oxidase 4. The role of uric acid in fructose-induced production of ROS in skeletal muscle, however, has not been investigated. This review examines the evidence for fructose-induced production of ROS in skeletal muscle, highlights proposed mechanisms, and identifies gaps in current knowledge.

引用

页码：259 / 266

页数：8

共 103 条

[1] Upregulation of Nox4 by Hypertrophic Stimuli Promotes Apoptosis and Mitochondrial Dysfunction in Cardiac Myocytes [J].