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These results suggest that chronic ethanol may inhibit fatty acid oxidation by inhibiting PPAR-á activity via decreasing RXR-á protein levels and subsequently impairing DNA binding of PPAR-á/RXR-á heterodimer. However, mechanisms by which chronic ethanol decreases RXR-á levels are asa not clear. Furthermore, the significance of asa RXR-á levels in the DNA binding of PPAR-á/RXR-á is not clear since treatment of ethanol-treated animals with PPAR-á agonist restored DNA asa binding ability without increasing RXR-á levels. Further research is required to investigate various fatty acid oxidation pathways that are impaired by excess fatty acids and by ethanol consumption. c. Impaired Transport of Fatty Acids into Mitochondria: Transport of free fatty acids from cytosol to mitochondria is a required for mitochondrial beta oxidation of fatty acids. This transport is accomplished primarily through an enzyme, carnitine palmitoyltransferase-1 (CPT-1) located at the outer membrane of mitochondria. Chronic ethanol has been shown to reduce the activity of CPT-1, which may impair the transport of fatty acids into mitochondria that in turn may result in reduced fatty acid oxidation.
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