Flashcards in TAG Degradation, FA Oxidation, Ketone body Review Slides Deck (21):
What hormone stimulates the conversion of triacylglycerol to fatty acids? Where does this occur?
Epinephrine- it stimulates the HSTL (hormone sensitive triacylglycerol lipase) to break down triacylglycerol into fatty acids
This is occurs in adipose tissue. Fats are stored as TAG's in adipose tissue, and are mobilized for energy by epinephrine.
How is biosynthesis of fatty acids affected by epinephrine?
Fatty acid biosynthesis is inhibited by epinephrine.
How is ketone body formation affected by epinephrine?
Ketone body formation is stimulated by epinephrine
How is gluconeogenesis affected by epinephrine?
Gluconeogenesis formation is stimulated by epinephrine
How is glycolysis affected by epinephrine?
Glycolysis is inhibited by epinephrine
Where does the oxidation of fatty acids occur?
Fatty acid oxidation (beta-oxidation) occurs in the mitochondrial matrix.
Free fatty acids cannot diffuse into the mitochondrial matrix for beta oxidation. How do they get there?
Fatty acids are converted to fatty acyl-CoA by Acyl-CoA synthase.
Carnitine then transports the fatty acid into the mitochondrial matrix using the carnitine palmitoyl transferase-1.
What form are fatty acids transported into mitochondrial matrix for beta oxidation?
What substance inhibits Carnitine palmitoyl transferase I? Explain.
Malonyl CoA is the product of the reaction catalyzed by acetyl-CoA carboxylase, the rate limiting enzyme in fatty acid biosynthesis. Therefore, high levels of malonyl CoA are indicative of high energy status.
How does decreased malonyl CoA affect fatty acid beta oxidation?
Decreased malonyl CoA increases fatty acid oxidation.
Where does ketone body formation occur?
Ketone body formation occurs in the liver
Where does ketone body utilization occur?
Everywhere except for the liver
Which is the rate-limiting enzyme in ketone body formation?
What is the rate limiting step in ketone body catabolism?
acetoacetate: succinyl CoA transferase (thiophorase)
What hormonal regulation stimulates the release of TAG's (in adipose tissue) into free fatty acids?
An increase in epinephrine and a decrease in insulin stimulates HSTLipase to cleave TAGs into their respective free fatty acids.
How do the free fatty acids from adipose tissue travel to the liver?
FFA's "surf" through the blood on albumin
Once in the liver, what happens to FFAs released from adipose tissue?
Once in the liver, FFAs are converted into Acyl-CoA. Acyl-CoA is then transferred into the into the inner mitochondrial matrix (on carnitine). Acyl CoA is then subsequently broken down into acetyl CoA's.
How does ketone body production start?
As fatty acid oxidation continues, ATP builds up in the cell and eventually inhibits the ETC. When the ETC slows down, NADH builds up and eventually stop the KREBS cycle. When the Krebs cycle stops, acetyl CoA builds up (because there is no allosteric regulation negatively inhibiting fatty acid oxidation). Acetyl CoA can then be shunted into the ketone body biosynthesis pathway
How does malonyl CoA affect the beta oxidation of fatty acids?
Malonyl CoA inhibits fatty acid oxidation. This makes sense, as malonyl CoA is an intermediate in fatty acid biosynthesis. It doesn't make sense to break down fatty acids and build them up at the same time.
Carbohydrates are broken down into acetyl CoA in the liver. What happens when citrate and insulin levels are high?
Acetyl CoA carboxylase (requires biotin) is inhibited.