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Lecture 22
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Lecture 22 objectives
Understand hormonal regulation of fatty acid mobilization
Understand how fats provide energy to the brain
Understand differences and similarities between starvation and
diabetes
Describe the reactions of fatty acid synthesis
Compare FAS and b-oxidation
Understand the regulation of fatty acid metabolism
Hormonal regulation
The brain problem…
Most energy stored as fatty acids
Brain only uses Glc
Fatty acids  Glc?
The TCA
The brain problem…
Most energy stored as fatty acids
Brain only uses Glc
Fatty acids  Glc?
How does brain function during starvation?
Production of ketone bodies
Starvation  Glycogen = 1 day
Amino acids  Glc. BUT…
Muscles can use fatty acids ( need for Glc)
Gluconeogenesis
Without
OAA, so
TCA
, liver makes “___________” from fats
Ketone bodies
Diabetes & ketone bodies
Starvation  __ KB  Used by brain
Extreme starvation  Muscle breakdown
No insulin  _ Blood sugar, AND _ FA breakdown
Too much Acetyl CoA  __ Ketone bodies
Brain has plenty of Glc!
__ Ketone bodies in blood = __ pH  __ Death
If only…
Making fatty acids = adding 2 Cs to chain!
AcCoA  Malonyl CoA
ACP in FAS
FAS
FAS
Fatty acid synthesis
Substrate shuttling in FAS
Substrate shuttling in FAS
Further steps…
Further steps…
Data analysis
Liraglutide is a drug that inhibits production of
Glucagon. Treat normal and diabetic mice with
Liraglutide and measure levels of blood glucose and
ketone bodies.
Normal Diabetic
-Liraglutide
+Liraglutide
Ketone bodies
-Liraglutide
+Liraglutide
Blood glucose
Glucagon levels
-Liraglutide
+Liraglutide
Normal Diabetic
Normal Diabetic
Regulation of FAS & breakdown
Allosteric regulation of ACC