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Exam 3 - Regulation

Regulation of metabolism

committed step of glycolysis F6P → F1,6-BP via PFK-1
enzymes regulated in glycolysis Hexokinase, PKF-1, Pyruvate Kinase
Hexokinase allosteric reuglation inhibited by G6P (feedback)
PFK-1 allosteric regulation Inhibited by ATP, low pH (mm), citrate (liver). Stimulated by AMP, F2,6-BP (made by conversion of F6P to F2,6BP by PFK-2).
Pyruvate Kinase allosteric reuglation Inhibited by ATP, alanine. Stimulated by F1,6-BP (last product of prep phase)
PFK-1 hormonal regulation Glucagon - activates PKA → phophorlates PFK-2 to inactivate it → FBPase2 decreases F2,6-BP → inhibition of glycolysis (no PFK-1 stim.) Insulin - removes phosphate from PFK-2 to activate it, allowing conversion of F6P to F2,6-BP → PFK-2 stimulated
enzymes regulated in gluconeogenesis Pyruvate carboxylase, PEP carboxykinase, F1,6-BPase
Pyruvate carboxylase allosteric regulation Inhibited by ADP. Stimulated by acetyl-CoA.
PEP carboxykinase allosteric regulation Inhibited by ADP
F1,6-BPase allosteric regulation Inhibited by AMP, F2,6-BP. Stimulated by citrate.
Why is alanine an allosteric inhibitor of Pyruvate Kinase (glycolysis) alanine can be converted into pyruvate via alanine aminotransferase. Since pyruvate is a subtrate of this PK, this will decrease the enzyme's activity
Glucagon's hormonal regulation of gluconeogenesis and glycolysis stimulates gluconeogenesis enzymes (PC, PEPCK, F1,6BPase,) inhibits glycolysis enzymes (Pyruvate kinase, PFK-1), and phosphorolates PFK-2 on PFK-2/FBPase-2 so FBAase-2 domain is active (decreases F2,6-BP to decrease PFK-1 stimulation)
Main mechanism that insulin controls gluconeogenesis and glycolysis increases gene expression of glycolysis enzmyes while decreasing the expresssion of gluconeogenesis enzymes
Flow of Pentose Phosphate shunt when the body needs Ribose-5-Phosphate for nucleotide biosynthesis. Non-oxidative branch backward (convert F6P from glycolysis to Ribose-5-Phosphate)
Flow of Pentose Phosphate shunt when the body needs Ribose-5-Phosphate and NADPH Oxidative branch forward (remove G6P from glycolysis and convert to Ribulose-5-Phosphate, producing 2 NADPH [and Co2]) (then run 1st step of nonox to convert ribulose-5-P to Ribose-5-P)
Flow of Pentose Phosphate shunt when the body needs NADPH only Oxidative and Nonoxidative forward and reverse of glycolysis [gluconeogenesis] (remove G6P and convert to Ribulose-5-P to make 2 NADPH) (run non-ox to produce Glyceraldehyde-3-P and F6P to run through gluconeogenesis to reproduce G6P and continue cycle)
Flow of Pentose Phosphate shunt when the body needs NADPH and ATP Oxidative and Nonoxidative and glycolysis forward (remove G6P to convert to Ribulose-5-P to produce 2 NADPH) (run nonox to produce F6P and Glyceraldehyde3-P to pump back into glycolysis) (run pay-off stage of glycolysis to produce 4 ATP and 2 NADH)
What are the 3 enzymes a part of the PDH complex? E1 = Pyruvate DH, E2 = Dihydrolipoly Transacetylase, E3 = Dihydrolipoly DH
PDH allosteric regulation (3 inhibitors) Inhibited by High energy state (NADH, Acetyl-CoA, ATP).
PDH regulation via PDH Kinase and PDH Phosphatase PDH Kinase phosphorolates PDH to INACTIVATE it. Pyruvate and ADP inhibit PDH-K and thus activate PDH. PDH Phosphatase removes Pi to activate Pi. Calcium (in mm) and Insulin (in liver and adipose) activate PDH-P and thus activate PDH
Alpha-Ketogluterate DH (TCA cycle) allosteric regulation (3 inhibitors) Inhibited by ATP, NADH, Succinyl-CoA
Isocitrate DH (TCA cycle) allosteric regulation (2 inhibitors, 1 stimulator) Inhibited by ATP, NADH. Stimulated by ADP
Alanine inhibits what enzyme? Pyruvate Kinase
Citrate and low pH inhibites what enzyme? PFK-1 (citrate activates FBPase-1)
What is the main enzyme of glycogen synthesis that is regulated? Glycogen synthase - Insulin dephosphorolates to activate, and Glucagon phosphorolates to activate
What is the main enzyme of glycogen breakdown that is regulated? Glycogen phosphorolase - Glucagon phosphorolates to (partially) activate (Ca2+ fully activates), and Insulin dephosphorolates to inhibit
Allosteric regulation of Glycogen Phosphorolase (and thus Glycogenolysis)in the liver and MM Liver - glucose binds active P-GP and inactivates it. MM - AMP binds GP and activates it; ATP and G6P bind P-GP amd inhibit it
Allosteric regulation of Glycogen Synthase G6P binds inactive GS-P and activates it.
Glucagon and Epinepherine work by activating PKA. What are the 5 targets of PKA and thier resulting effect? 1-Peripillin/HSL - increase FA release. 2-Gm on PP-1 and PP-1 inhibitor - prevents reversal of PKA. 3-Glycogen Synthase - inhib glycogen synthesis. 4-Phosphorolase Kinase- stim glycogenolysis (via GP) 5-PFK2 - stim. gluconeogenesis & inhib. glycolysis
What are the 2 DIRECT targets of Insulin that get phosphorolated? 1-Insulin Sensitive Kinase - phosphorolates Gm activator on PP-1 2-IRS-1 - activates PI-3K to convert PIP3 to PIP2 to activate PKB/Akt to phos/inactive GS-Kinase (thus prevent the phos/inactivation of GS → no shut-down of glycogen synthesis)
What are the 4 targets of protein-phosphatase-1 (PP-1) that get dephosphorolated and what effects do they have? 1-PFK-2 - stimulates glycolysis and inhibits gluconeogenesis 2-peripellin/HSL - decrease FA release 3-GP and Phosphorlase Kinase - inhibit glycogen breakdown 4-GS - stimulate Glycogen synthesis
Major and Minor means of regulation FA oxidation MAJOR -inhibition of CPT1 by Malonyl-CoA (intermediate in FA synthesis). MINOR -Inhibition of hydroxyacyl-CoA by high ratio of NADH/NAD+. And Inhibition of Thiolase by acetyl-CoA
Regulation of FA biosynthesis Acetyl-CoA Carboxylase - Glucagon activates AMPK or PKA to phosphorolate/inactivate. Insulsin activates PP2A to dephosphorolate/activate.
Acetyl-CoA Carboxylase (ACC) allosteric regulation Citrate binds P-ACC to activate. Palmitoyl-CoA binds ACC to inactivate. AMP stimulates AMPK to inhibit ACC. ATP inhibits AMPK to stimulate ACC.
Short-term regulation of the urea cycle Acetyl-CoA and Glutamate combine to form N-Acteylglutamate. This is stimulated by Arg. N-Acetylglutamate stimulates carbamyol phosphate synthase I
De Novo Pydimidine Synthesis Regulation Asp Transcarbamylase: CTP inhibits and ATP stimulates
De Novo Purine Synthesis Regulation (1) IMP DH: GMP inhibits and ATP stimulates. (2) Adenylsuccinate Synthase: AMP inhibits and GTP stimulates
Deoxyribonucleotide Synthesis Regulation (1) Active Site - dATP turns off, ATP turns on. (2) Specificity Site - dATP ↑ Pyr specificity, dPry ↑TTP which ↓Pyr & ↑GDP specificity, dGTP ↑ADP specificity
Serine Synthesis Regulation Serine inhibits 3-PG DH
Cholesterol storage (i.e. cholesterol ester formation) regulation Cholesterol stimulates ACAT
4 modes of regulation of cholesterol synthesis 1- Insulin activates, Glucagon deactivates HMG-CoA Reductase. 2- High sterols/cholesterol → UB-degradtion of HMG-CoA Reductase. 3- cholesterol binds SCAP which binds SREBP (HMG-CoA Reductase TF) to inhibit. 4- Mevaolonate inhibits HMG-CoA reductase
Created by: c.phill