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Increase in oxidative stress due to long-term hyperglycemia is believed to augment proinflammatory protein levels, angiotensin II, protein kinase C activation, and transforming growth factor-beta (TGF-) expression
Adenovirus-mediated overexpression of CD36 enhances hepatic fatty acid uptake and fat accumulation [22], while liver-specific knockout of CD36 decreases hepatic lipid levels in both genetic and diet-induced steatosis [23]
Several transgenic models have been generated with changes in DAT expression or function or mutations in the DAT gene (386)
References 1 RussoMPGrande-RattiMFBurgosMAMolaroAABonellaMB
