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Fatty acid catabolism 1. Digestion, Mobilization, and Transport of Fatty acids 2. b Oxidation 3. Ketone Bodies Digestion of dietary lipids in vertebrates glucagon Mobilization of triacylglycerols stored in adipose tissue β Oxidation of fatty acids-the free fatty acids that enter the cytosol from the blood cannot pass directly through the mitochondrial membranes 1. Acyl-CoA synthetases : Fatty acid +CoA + ATP → fatty acyl-CoA + AMP + PPi isozymes for short, intermediate, or long chainfatty acids 2. Carnitine acyl transferase I - acyl-carnitine/carnitine transporter - carnitine acyltransferase II: Complete oxidation of fatty acids into CO2 and ATPβ oxidation, TCA cycle, electron transport chain LCAD C 12-18 MCAD C 4-14 SCAD C to 8 (AD) The βoxidation of palmitoyl CoA Genetic mutation of MCAD causes serious diseases Palmitoyl-CoA + 7 CoA + 7 FAD + 7 NAD+ + 7 H2O 8 actyl-CoA + 7 FADH2 + 7 NADH + 7 H+ Coordinated regulation of fatty acid synthesis and oxidation [NADH]/[NAD+] [Acetyl-CoA] Ketone Bodies - formed in the liver and oxidized in skeletal and heart muscle and the renal cortex. Brain adapts to use them under starvation conditions Ketone body formation in liver in mitochondria matrix in cytosol for cholesterol synthesis Ketone body oxidation Extrahepatic tissue Untreated diabetes, severe dieting, fasting promote gluconeogenesis, slow the citric cycle (by drawing off oxaloacetate) and enhance the conversion of acetylCoA to acetoacetate. • Ketone bodies in the blood and urine of untreated diabetics can reach extraordinary levels, a condition called ketosis. • In individuals on every low-calorie diets, using the fats stored in adipose tissue as their major energy source, levels of ketone bodies in the blood and urine must be monitored to avoid the dangers of acidosis and ketosis (ketoacidosis).