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 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).