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).
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