Fatty acid catabolism 1.Digestion, Mobilization, and Transport of Fatty acids  Oxidation 3. Ketone Bodies.

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Fatty acid catabolism 1.Digestion, Mobilization, and Transport of Fatty acids  Oxidation 3. Ketone Bodies

Digestion of dietary lipids in vertebrates

Mobilization of triacylglycerols stored in adipose tissue glucagon

β Oxidation of fatty acids- the free fatty acids that enter the cytosol from the blood cannot pass directly through the mitochondrial membranes isozymes for short, intermediate, or long chain- fatty acids 2. Carnitine acyl transferase I - acyl-carnitine/carnitine transporter - carnitine acyltransferase II: 1.Acyl-CoA synthetases : Fatty acid +CoA + ATP → fatty acyl-CoA + AMP + PPi

Complete oxidation of fatty acids into CO 2 and ATP- β oxidation, TCA cycle, electron transport chain

The βoxidation of palmitoyl CoA LCAD C MCAD C 4-14 SCAD C to 8 (AD) Palmitoyl-CoA + 7 CoA + 7 FAD + 7 NAD H2O 8 actyl-CoA + 7 FADH2 + 7 NADH + 7 H + Genetic mutation of MCAD causes serious diseases

[NADH]/[NAD+] [Acetyl-CoA] Coordinated regulation of fatty acid synthesis and oxidation

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

in mitochondria matrix Ketone body formationKetone body oxidation in liverExtrahepatic tissue in cytosol for cholesterol synthesis

Untreated diabetes, severe dieting, fasting promote gluconeogenesis, slow the citric cycle (by drawing off oxaloacetate) and enhance the conversion of acetyl- CoA 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).