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dc.contributor.authorMadlala, Hlengiwe P.
dc.contributor.authorMaarman, Gerald J.
dc.contributor.authorOjuka, Edward
dc.date.accessioned2023-01-20T07:02:44Z
dc.date.available2023-01-20T07:02:44Z
dc.date.issued2016
dc.identifier.citationMadlala, H. P., Maarman, G. J., & Ojuka, E. (2016). Uric acid and transforming growth factor in fructose-induced production of reactive oxygen species in skeletal muscle. Nutrition reviews, 74(4), 259-266.en_US
dc.identifier.uridoi: 10.1093/nutrit/nuv111
dc.identifier.urihttp://ir.lirauni.ac.ug/xmlui/handle/123456789/485
dc.description.abstractThe 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 b1 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.en_US
dc.language.isoenen_US
dc.publisherOxford University Pressen_US
dc.subjectfructose, mitochondrial dysfunction, reactive oxygen species, transforming growth factor, uric acid.en_US
dc.titleUric acid and transforming growth factor in fructose-induced production of reactive oxygen species in skeletal muscleen_US
dc.typeArticleen_US


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