Fatty acid catabolism

1. Digestion, Mobilization, and Transport of Fatty acids Oxidation3. 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 CO2 and ATP- β oxidation, TCA cycle,electron transport chain

The βoxidation of palmitoyl CoA

LCAD C 12-18 MCAD C 4-14 SCAD C to 8 (AD)

Palmitoyl-CoA + 7 CoA + 7 FAD + 7 NAD+ + 7 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 formation Ketone body oxidation

in liver Extrahepatic 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).