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What is glycogen synthase activated and inhibited by?
What about glycogne phosphorylase (3,3)
Glucagon, AMP, Ca2+. Insulin (PP1), glucose ATP
ALT - what does it do?
Transfers a-amino group from alanine to a-ketoglutarate to form pyruvate and glutamate.
AST - what does it do?
Transfers amino group from glutamate to OAA forming aspartate.
Glutamate --> a-ketoglutarate + free NH3
What regulates the urea cycle? (4)
Activated by high protein diet, starvation (upregulates autophagy and urea cycle enzymes), high protein meal with arginine (activates N-acetylglutamate which activates CPS-1)
In lipoproteins, what does APOCII do? LPL? ABC transporters? LCAT? CETP? ACAT? ApoE? Can ApoB48 bind to LDL-R?
- APOCII activates LPL (activated by insulin).
- LPL = lipoprotein lipase - hydrolyzes TAGs in chylomicrons & VLDL for uptake into cell (increased in pregnant womenin 3rd trimester & cancer patients
- ABC transporters - Help HDL remove free cholesterol from plasma mebranes of peripheral tissues to return to liver.
- LCAT - Esterifies cholesterol --> CE in HDL Activated by ApoA2
- CETP - cholesterol ester transfer protein - transfers TAGs.
- ACAT - esterifies CE within cell. Activated when cell levels of cholesterol are high
- ApoE - ligand for binding IDL, LDL to LDL-R and LRP
- No. Needs help from ApoE.
HMG CoA Reductase
Activated by (2)
Inhibited by (4)
Activated by low levels of sterols --> SREBP2 and insulin.
Inhibited by glucagon, AMPK, cholesterol feedback, and statin drugs.
Succinyl CoA acetoacetate transferase
Activates acetoacetate into its active form (acetyl CoA) for use in peripheral tissues. Not found in liver!
How is ketone body formation regulated?
Emzyme Activated by? (2) Inhibited by? (4)
- 1. Magnitude of lipolysis (amount of FAs released from adipocytes)
- 2. CPT-1 and entry of acetyl CoA into mitochondria
- 3. Entry of acetyl CoA --> TCA cycle (lack of entry increases substrates for ketone body formation)
- 4. HMG CoA reductase activated by SREBP-2 and insulin.
- 5. Inhibited by glucagon, AMPK, cholesterol (feedback inhibition) and statin drugs.
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