Metabolism Flashcards
When [ammonia] is high, what else will be elevated?
[glutamine]
What cofactor does transamination require?
Pyridoxal phosphate, a B6 derivative
What stimulates proteolysis?
increased [cortisol]
What stimulates the activity of PFK1?
Increased [AMP]
Increased [insulin]
What inhibits the activity of PFK1?
Increased [ATP]
Increased [citrate] (synthesized during FA synthesis when energy stores are high)
Increased [glucagon]
How are NADH and FADH2 produced?
TCA + glycolysis.
Used in oxidative phosphorylation (ETC)
How does a salicylate overdose interrupt metabolic function?
Via uncoupling the synthesis of ATP from the ETC. Proteins create channels or carry H+ across the mitochondrial membrane, dissipating the proton gradient. E- still flow through the ETC complexes, but generate no ATP. Results in increased heat production, increased [ADP], and increased metabolic rate.
Same mechanism as brown fat and dinitrophenol.
How does cyanide interrupt metabolic function?
By inhibition: bonding to complex IX results in a stop of flow of electrons, which in turn causes NADH and FADH2 to accumulate but produces no ATP.
Which intermediate of the TCA cycle is involved in the production of amino acids?
a-ketoglutarate (via glutamate hydrogenase), as well as oxaloacetate
Which amino acids are anaplerotic?
Isoleucine and valine: convert to propionyl CoA –> succinyl CoA
How can fatty acids join the TCA cycle?
Odd-chain fatty acids undergo b-oxidation, producing acetyl coA + propionyl coA. Propinoyl CoA can convert to succinyl coA and join the TCA cycle ( the acetyl coA can combine with oxaloacetate and also join).
What is B12 essential for?
Oxidation of odd-chain length fatty acids.
What would be an indicator that someone is low in B12?
An accumulation of methylmalonic acid (a sign of pernicious anemia)
What is the most important anaplerotic enzyme?
Pyruvate carboxylase, which can generate more oxaloacetate from pyruvate
What kind of bonds create the branches in glycogen?
a-1-6-glycosidic bonds
What kind of bonds create the backbone of glycogen?
a-1-4-glycosidic bonds
Describe the movement of acetyl coA during fatty acid synthesis.
Acetyl coA can’t move out of the mitochondria into the cytoplasm on its own. It combines with oxaloacetate to become citrate. If [ATP] is high, the TCA cycle will slow and citrate will accumulate, leading to citrate diffusing out of the mitochondria. Once in the cytoplasm, it undergoes a reaction to become acetyl coA again (and the oxaloacetate returns to the mitochondria).
Describe the regulation of fatty acid oxidation.
Malonyl coA is an intermediate of fatty acid synthesis. It acts as an inhibitor of CPT1, which prevents fatty acyl coA from entering the mitochondria for oxidation.
Describe the regulation of fatty acid synthesis.
Acetyl coA carboxylase is the tightly regulated enzyme of interest in fatty acid synthesis.
Insulin causes PP2 to REMOVE phosphate group from acetyl coA carboxylase which ACTIVATES it. Insulin Increases activity.
Glucagon causes AMPPK to phosphorylate acetyl coA carboxylase, which DEactivates it. Glucagon decreases. increased [ATP] will also inhibit activity.
ATP, biotin, and CO2 is necessary for acetyl coA carboxylase to convert acetyl coA –> malonyl coA.
When [acetyl coA] is high, how are fatty acids affected?
Thiolase will convert acetyl coa into acetoacetyl coA, which can convert to acetoacetate.
Acetoacetate is a ketone body.
If [NADH] is high in the liver, the acetoacetate will be converted to b-hydroxybutyrate, which will (along with some acetoacetate) will move to circulation.
