ATP yield from beta-oxidation of saturated fatty acid, beta-oxidation of odd-carbon fatty acids and ketone bodies

1. Lipid Metabolism
Part 2

2. Energy Yield from Oxidation of FA
• FADH2, NADH & Acetyl-CoA released in β-oxidation of fatty acids are used in
generating ATP
• Stearic acid(C-18) will be considered.
# AcetylCoA =
#𝐂
𝟐
# Cycles/spirals = #Acetyl-CoA -1
# Cycles/spirals = #NADH = #FADH2
AcetylCoA = 10 ATP
NADH = 2.5 ATP
FADH2 = 1.5 ATP

3. ATP Yield from Oxidation of Stearic Acid
Name of Specific Process Amount & Energy
currency
Total ATP
Equivalent
Total ATP

4. • Not frequently encountered but undergo -oxidation
• -oxidation gives several molecules of acetyl-CoA
•
𝐧 −𝟑
𝟐
where n = the number of carbon
• Last -oxidation cycle of produces one molecule of propionyl-CoA
• Propionyl-CoA is converted to succinyl-CoA via methyl malonyl-CoA
• Succinyl-CoA is an intermediate of TCA
• Catabolism of some amino acids yields propionyl-CoA & methyl
malonyl-CoA
-Oxidation of Odd Number FA

5. -Oxidation of Odd Number FA

6. Oxidation of Monounsaturated FA
• Cis-trans isomerization is needed to convert
monounsaturated fatty acids to acetyl-CoA
• Oxidation of unsaturated fatty acids does not
generate as many ATPs when compared to
saturated fatty acids with the same number of
carbons
• The double bonds results to skipping some step 1

7. Ketone Bodies
• Formed when the amount of acetyl-CoA produced is excessive when
compared to the amount of oxaloacetate available to react with it
• Starvation causes an organism to break down fats for energy, leading to
the production of large amount of acetyl-CoA by -oxidation
• In diabetic patients, cause of imbalance is inadequate intake of
carbohydrates
• Formed principally in liver mitochondria
• Ketone bodies - Acetone, -hydroxybutyrate, and acetoacetate
• Source of fuel for brain, muscle and heart during starvation
• Acetoacetate can be used as a fuel in most tissues and organs

8. Ketone Bodies

9. Ketone Bodies & Diabetes
• Glucose is abundant in blood, but uptake by cells in muscle, liver, and
adipose cells is low
• Cells, metabolically starved, turn to gluconeogenesis and fat/protein
catabolism
• In type I diabetics, oxaloacetate is low, due to excess gluconeogenesis, so
acetyl-CoA from fat/protein catabolism does not go to the TCA cycle, but
rather to ketone body production
• Acetone can be detected on breath of type I diabetics