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AMPK
A WIDE VARIETY OF ACTIVITIES.
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Glycogenesis
Glycogen synthase
Rate-determining enzyme for glycogenesis.
Activated by insulin (PP1); inhibited by PKA (via cAMP & glucagon/epinephrine)
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Branching Enzyme
Glycogenesis
Chops off 6-8 glucoses off of the linear chain and attaches as a1,6 bond as branch.
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Glycogen phosphorylase
Rate-det enzyme for glycogenolysis
Activated by PKA, cAMP, glucagon/ep. Inhibited by insulin (PP1)
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Glucosyl transferase
- Glycogenolysis
- Responsible for cutting off 3 glucose units on a 4 glucose chain and transferring them to linear branch so that glycogenolysis can continue.
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Debranching Enzyme
Glycogenolysis:
Chops off a1,6 bond - last glucose - and releases as free glucose.
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Glucose 6 Phosphatase
- Glucose 6 P--> free glucose.
- Seen in glycogenolysis, gluconeogenesis
Not in muscle!
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PKA
Glucagon/Epinephrine --> activate adenylyl cyclase to synthesize cAMP which activates synthesis of PKA. Seen in many metabolic rxns.
- - Glycogenolysis/glycogenesis
- - Gluconeogenesis
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Protein Phosphatase 1
Activated by insulin
Seen in both glycogen metabolism
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Ca2+-dep kinase
Seen in muscle during glycogenolysis.
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Glucokinase vs. Hexokinase?
- Km?
- Vmax?
- Tissues?
- Activation/Inhibition?
- What is important about glucokinase's Vmax?
Glucokinase has higher km (specificity) and higher capacity to process glucose
Glucokinase is found in the liver while hexokinase is found in most tissues.Activated by glucose
Glucokinase has a high Vmax, allowing liver to remove lots of glucose from blood post-prandially to prevent hyperglycemia.
Glucokinase has absolutely no feedback inhibition, while hexokinase is allosterically inhibited by G6P (fastest regulation).
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PFK-1
- Activated by: AMP, F2,6BP
- Inhibited by: ATP, citrate
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Pyruvate kinase
Glycolysis: PEP---> Pyruvate
Inhibited by glucagon
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Glucose 6 dehydrogenase
Main enzyme in PPP
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Pyruvate carboxylase
Substrate --> product?
Requires?
Is this enzyme found in muscle? If so, what's the diff?
Activated by? Inhibited by? 1 each.
- Pyruvate --> OAA
- Requires B7
- Yes, but muscle does not do GNG - instead pyruvate carboxylase is used to make OAA for TCA cycle for oxidative phosphorylation.
Activated by: Acetyl CoA (elevated levels of acetyl CoA signal metabolic state in which more OAA is needed - when OAA is needed for synthesis of glucose in liver & kidney). At low levels of Acetyl CoA --> PDH is active for TCA cycle.
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PEPCK
Driven by?
Regulation of PEPCK?
- OAA --> PEP
- Driven by GTP (combined actions of pyruvate carboxylase & PEPCK --> energetically favorable pathway from pyruvate --> PEP).
Gene transcription regulated by glucagon:insulin ratio. Glucagon increases PEPCK.Adiponectin & insulin decrease PEPCK
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F1,6bisphosphatase
Activated by? 3
Inhibited by? 3
F1,6BP --> F6P
- Activated by: (1)ATP, (2) glucagon (cAMP, PKA, p'lated form of PFK-2/FBP-2 allows FBP2 domain to be active. Decreased levels of F2,6BP decreases inhibition of F1,6BPtase, increasing GNG.
- Inhibited by: AMP, insulin, (PFK-2 --> F2,6BP).
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Glucose-6-Phosphatase
Found in which 2 organs?
Regulation?
- Glucose 6 P --> Free glucose.
- - Found only in liver and kidney
Adiponectin decreases its gene transcription
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HMG CoA Synthase
Acetyl CoA + acetoacetate --> HMG CoA
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HMG CoA Reductase
Regulation?
HMG CoA --> Mevalonate - Rate limiting enzyme for cholesterol synthesis.
Sterols are dependent on regulation of gene expression (SREBP-2 binds to SRE of reductase gene).
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ACAT/LCAT
Esterifies cholesterol into cholesteryl esters.
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