Term
| Describe the key factors regulating adipose tissue lipolysis |
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Definition
Hormone-sensitive lipase
- activated when phosphorylated by cAMP-dependent protein kinase; cAMP is made when hormones (e.g. epi, glucagon) bind & activate adenylyl cyclase
- because acetyl CoA carboxylase is inhibited by hormone-directed phosphorylation when the cAMP-mediated cascade is activated, FA synthesis is turned OFF when TAG degradation is turned ON
In the presence of high insulin and glucose, HSL is dephosphorylated, and becomes inactive
The free (unesterified) FA move through adipocyte cell membrane -> bind to albumin in plasma -> tissues -> acyl CoA -> oxidized for energy in tissues |
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Term
| Describe the basic chemical features of beta-oxidation of FA |
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Definition
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Term
Fed state - hormonal regulation (adipose tissue)
(image) |
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Definition
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Term
| Discuss the role of ketone bodies in energy metabolism |
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Definition
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Term
| Regulation of FA oxidation |
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Definition
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Term
| Regulation of fatty acid metabolism |
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Definition
Availability of FA from adipose tissue lipolysis
Transport of fatty acyl CoA into mitochondrial matrix
- down-regulation of carnitine acyltransferase by malonyl-CoA (prevents futile cycling)
Availability of coenzymes (NAD, FAD) to promote beta-oxidation |
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Term
Production of ketone bodies
(muscle vs. liver) |
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Definition
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Term
| Fasted state - adipose cell (image) |
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Definition
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Term
What is beta-ox of FA?
- how does fatty acyl CoA enter the mitochondrial matrix? |
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Definition
The major pathway for catabolism of saturated FA
A mitochondrial pathway, in which two-C fragments ore successively removed fatty acyl CoA -> acetyl CoA, NADH, FADH2
The carnitine shuttle transports the long-chain acyl from the cytosol into the mitochondrial matrix (rate-limiting)
[image] |
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Term
7 repetitions of beta-oxidation
ATP yield?
- from NADH, FADH2
- acetyl CoA
- TCA cycle
- total ATP yield? |
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Definition
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Term
| Fatty acid metabolism in the liver |
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Definition
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Term
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Definition
The major pathways utilizing acetyl-CoA are the TCA cycle and fatty acid synthesis.
Fatty acid synthesis is preferred in the fed state (cytosol).
During fatty acid oxidation in the fasted state, liver is flooded with FA mobilized rom adipose tissue.
Acetyl-CoA (produced primarily by FA degradation) inhibits pyruvate deHase/activates pyruvate carboxylase, and may accumulate in the mitochondria beyond the capacity of the TCA cycle. Then it is converted into ketone bodies (ketogenesis) - an overflow pathway.
The OAA produced is used by the liver for gluconeogenesis rather than for the TCA cycle
Major ketone bodies: acetoacetate, β-hydroxy butyrate, acetone |
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