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thus decreasing the rate of de novo fatty-acid biosynthesis and increasing rates of mitochondrial ^-oxidation and ketogenesis. Insulin effects are mediated through activation of its receptor tyro-sine kinase and are in general opposite to those of glucagon, stimulating glycolysis and fatty-acid synthesis while inhibiting fatty-acid degradation. Insulin and glucagon have both acute and long-term effects on fatty-acid metabolism. The transcription factor SREBP1c is thought to mediate the action of insulin in upregulating genes involved in fatty-acid synthesis. Activation of PPARa on the other hand increases rates of fatty-acid oxidation and ketogenesis. Endogenous ligands for this nuclear receptor are thought to include polyunsat-urated fatty acids and branched-chain fatty acids. The PPARs heterodimerize with the retinoid X receptor, and both receptors must be ligand-bound for transcriptional activation. Several mito-chondrial, microsomal, and peroxisomal genes associated with fatty-acid catabolism are upregu-lated via PPARa stimulation.

See also: Cholesterol: Sources, Absorption, Function and Metabolism; Factors Determining Blood Levels. Fatty Acids: Monounsaturated; Omega-3 Polyunsaturated; Omega-6 Polyunsaturated; Saturated; Trans Fatty Acids. Lipids: Chemistry and Classification; Composition and Role of Phospholipids. Obesity: Definition, Etiology and Assessment.

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