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

被引:31
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
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
收藏
页码:259 / 266
页数:8
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