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Various mechanisms have symptoms of nonalcoholic fatty liver diseasee been proposed for this effect. A redox shift resulting in increased ratio of NADH/NAD+ has been implicated in the development of fatty liver via inhibition of mitochondrial fatty acid beta oxidation and tricarboxylic acid cycle. However, normalization of redox state symptoms of nonalcoholic fatty liver diseasee failed to attenuate alcohol-induced fatty liver, suggesting that other mechanisms may also be contributing to this condition. Alcohol and excess fatty acids may also impair fatty acid oxidation by inhibiting the activities of enzymes involved in fatty acid oxidation. Peroxisome proliferators-activated receptor alpha (PPAR-á) is a member of the nuclear hormone receptor super family, symptoms of nonalcoholic fatty liver diseasee which when dimerized with retinoid X receptor alpha (RXR-á) regulates transcription of a set of genes involved in the oxidation and transport of fatty acids.
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