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Quiz 8 Study Guide

by: Skyler Tuholski

Quiz 8 Study Guide BCMB 3100

Skyler Tuholski
GPA 4.0

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I compiled a study guide that covers the important book material from chapters 17,18, and 19 as well as highlights from the powerpoints and conceptual questions discussed in lecture and breakout. D...
Intro to Biochem and Molecular Bio
Wood & Sabatini
Study Guide
gluconeogenesis, citric acid cycle
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This 16 page Study Guide was uploaded by Skyler Tuholski on Friday September 30, 2016. The Study Guide belongs to BCMB 3100 at University of Georgia taught by Wood & Sabatini in Fall 2016. Since its upload, it has received 129 views. For similar materials see Intro to Biochem and Molecular Bio in Biochemistry at University of Georgia.


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Date Created: 09/30/16
Ch 17: Gluconeogenesis and Ch’s 18 & 19: The Citric Acid Cycle Ch 17 notes:  Gluconeogenesis: synthesis of glucose from noncarbohydrate precursors o Takes place in liver and kidney to maintain blood glucose concentration so the brain and muscle can extract glucose as needed  Converts pyruvate into glucose  Noncarbohydrate precursors of glucose are first converted into pyruvate o Major noncarbs: lactate, amino acids, glycerol o Lactate is converted into pyruvate in the liver by lactate dehydrogenase o Amino acids come from dietary protein and muscle breakdown o Glycerol comes from the hydrolysis of triacylglycerols and can enter either the glycolysis or gluconeogenesis pathway  Gluconeogenesis is not a complete reversal of glycolysis o Most of the free energy in glycolysis takes place in the 3 irreversible steps (1- hexokinase, 3-phosphofructiokinase, and 10-pyruvate kinase) o In gluconeogenesis, the irreversible rxns of glycolysis are bypassed Gluconeogenesis Net Reaction: Input: 2 Pyruvate + 4 ATP + 2 GTP + 2 NADH + 2 H + 6 H O 2 Yields  Glucose + 4 ADP + 2 GDP+ 2 NAD + 6 Pi  Carboxylation of pyruvate to form oxaloacetate  This first step of gluconeogenesis occurs in the mitochondria  Requires 1 ATP  Catalyzed by pyruvate carboxylase o Requires biotin, a covalently attached prosthetic group that serves as the carrier of activated CO2 o Biotin is not carboxylated unless acetyl CoA is bound to the enzyme  Oxaloacetate is shuttled to cytoplasm and converted to phosphoenyl pyruvate o Oxaloacetate reduced to malate by malate dehydrogenase and then transported across mitochondrial membrane, where it is reoxidized to oxaloacetate o Going from oxaloacetate to malate yields NADH o Oxaloacetate is then simultaneously decarboxylated and phosphorylated by the enzyme PEP carbokinase to generate PEP. o Decarboxylations often drive rxns that are otherwise highly endergonic  Conversion of Fructose 1,6-bispohosphate into Fructose 6-phosphate  PEP is then metabolized by the same enzymes of glycolysis, but in the reverse direction.  The rxns are near equilibrium, so when gluconeogenesis is favored, rxns proceed until the next irreversible step is reached st  *1 irreversible step: hydrolysis of fructose 1,6-bisphosphate into fructose 6-phosphate and ???? by????enzyme fructose 1,6-bisphosphatase o Large - G, allosteric enzyme that regulates gluconeogenesis  Generation of free glucose is important control point o Fructose 6-phosphate is converted to glucose-6 phosphate. In most cases, gluconeogenesis ends here. Free glucose is not generated; glucose 6- phosphate is converted into glycogen for energy storage o If it continues, glc 6-phosphate is transported to the lumen of the endoplasmic reticulum, where it is hydrolyzed to glucose by glucose 6- phosphatase. Glucose and Pi are shuttled back into cytoplasm.  Six phosphoryl groups are spent in synthesizing glucose from pyruvate o Only 2 ATP are used in the reversal of glycolysis o Example of coupling: 4 extra phosphoryl-transfer molecules are needed to turn an energetically unfavorable process (reversal of glycolysis) into a favorable one (gluconeogenesis) pg 319  Gluconeogenesis and Glycolysis are reciprocally regulated- within a cell, one pathway is more inactive while the other is more active. o Rate of glycolysis determined by concentration of glucose o Rate of gluconeogenesis determined by concentrations of lactate and other precursors of glucose o High glucose= glycolysis more active. Low glucose= gluconeogenesis more active o If they occur at the same time within a cell, it’s a futile cycle- you are just burning ATP and producing heat  Regulated with the interconversion of fructose 6-phosphate and fructose 1,6- bisphosphate o High AMP, low citrate  stimulates phosphofructokinase: glycolysis on  inhibits fructose 1,6-bisophosphate: gluconeogenesis off o High ATP, high citrate  inhibits phosphofructokinase: glycolysis off  stimulates fructose 1,6-bisophosphate: gluconeogenesis on  Also regulated in the liver with the interconversion of phosphoenolpyruvate and pyruvate o Pyruvate kinase inhibited by ATP and alanine: glycolysis off o Pyruvate carboxylase of gluconeogenesis is inhibited by ADP, activated by acetyl CoA  Regulation of PFK-2 o In high concentrations, fructose 6-phosphate activates the enzyme phosphofructokinase (PFK) through an intermediary, fructose 2,6- bisphosphate: activates glycolysis o Low concentration of glucose: fructose 2,6-bisphosphate dephosphorylated to fructose-6 phosphate, which no longer binds PFK: inhibits glycolysis o Fructose 2,6-bisposphate is formed from fructose 6-phosphate in a rxn catalyzed by PFK-2 o *key regulation in the liver o *Glucagon stimulates protein kinase A (PKA) when blood glucose is scarce, FBPase 2 is activated, glycolysis is inhibited and gluconeogenesis is stimulated o *High levels of fructose 6-phopsphate stimulate phosphoprotein phosphatase. PFK-2 is activated, glycolysis is stimulated and gluconeogenesis is inhibited  The Cori Cycle o Lactate formed by active muscle is converted into glucose by the liver. This cycle shifts part of the metabolic burden from the muscle to the liver o Provides temporary and readily available supply of Glc to muscle (exercise) and regenerates NAD+ to allow glycolysis to continue in anaerobic conditions Ch 18 Notes: Preparing for the Citric Acid Cycle  Review: pyruvate  lactic acid or ethanol (anaerobic fermentation) Pyruvate  Acetyl CoA (aerobic) then enters CAC  Overview of CAC: two-carbon acetyl units are oxidized to form 2 molecules of CO2, one molecule of ATP, and high-transfer-potential electrons  Pyruvate is oxidatively decarboxylated by pyruvate dehydrogenase complex to form acetyl CoA o Glycolysis happens in cytoplasm, CAC is in mitochondria o The irreversible conversion of pyruvate into acetyl CoA is the link between glycolysis and CAC o The pyruvate dehydrogenase complex is made up of 3 distinct enzymes  Synthesis of Acetyl CoA from pyruvate requires 3 enzymes and 5 coenzymes (aka prosthetic group) 1) Pyruvate dehydrogenase 2) Dihydrolipoyl transacetylase 3) Dihydrolipoyl dehydrogenase a. Catalytic Coenzymes: TPP, lipoic acid, FAD b. Stoichiometric coenzymes: CoA, NAD+ Three Steps to convert pyruvate into Acetyl CoA 1) Decarboxylation: Pyruvate combines with the carbanion form of TPP and is decarboxylated to yield hydroxyethyl-TPP. Rate-limiting Step. E 1 2) Oxidation: Hydroxyethyl group on TPP is oxidized to form acetyl group while being simultaneously transferred to lipoamide. Results in formation of high energy thioester bond in acetyllipoamide E 2 3) Formation of Acetyl CoA: E2 uses the energy of the thioester bond to transfer the acetyl group of acetyllipoamide to CoA. E 2  Pyruvate dehydrogenase complex cannot complete another catalytic cycle until dihydrolipoamide is oxidized to lipoamide. In doing so, 2 electrons are transferred to an FAD prosthetic group and then to NAD+ Lecture Question- What’s the advantage of organizing the enzymes of the pyruvate dehydrogenase into a single massive complex??  Allows for efficient transfer of the product of one reaction to the next enzyme to act as the substrate: active site proximity.  Minimizes side reactions and increases rate of overall reaction.  Enzymes are present in correct stoichiometric amounts.  It allows for efficient regulation of the phosphatase and kinase present  Pyruvate dehydrogenase complex is regulated by 2 Mechanisms o Key means of regulation of the complex in eukaryotes is covalent modification: phosphorylation 1) Pyruvate dehydrogenase (PDH) kinase switches off activity of the complex by phosphorylating E1 2) Deactivation is reversed by PDH phosphatase o Formation of acetyl CoA from pyruvate is an irreversible step in animals- cannot convert it back to glucose  Acetyl CoA has 2 fates:  Oxidation to CO2 by the citric acid cycle  Incorporation into lipid o Pyruvate dehydrogenase is switched off when the energy charge is high  High NADH and acetyl CoA activate the kinase deactivation of complex  High NAD, HS-CoA, Pyruvate inhibit the kinase allow production of acetyl CoA Lecture Question- What would happen if a person had a phosphatase deficiency?  Lots of inactive form of the PDH complex because it is always phosphorylated. Cannot convert pyruvate to acetyl CoA. Must take anaerobic path: results in a condition called lactic acidosis. Buildup of lactic acid in the blood is harmful, but your body does this to regenerate NAD+ to continue glycolysis.  Solution is a ketogenic (high fat, adequate protein, low carb) diet to minimize need to metabolize glucose. Instead, the body breaks down fatty acids to make acetyl CoA and continue citric acid cycle.  Increase of ATP continues glycolysis and furthers lactic acidosis. Mostly affects central nervous system since the CNS depends solely on glycolysis.  Disruption of Pyruvate Metabolism is the cause of Beri Beri o Caused by dietary deficiency of thiamine (vitamin B-1) o Insufficient PDH complex activity b/c TPP, the prosthetic group of E1, can’t be formed  you have a dead enzyme and lactic acidosis will occur o Big problem in Asia b/c polished rice is low in thiamine o Damage to peripheral nervous system: pain in limbs, weak muscles, damage to sensory nerves o Alcoholics with a poor diet can also suffer from beri beri o TPP is also found in α-ketoglutarate dehydrogenase (enzyme in the CAC), so beri beri leads to elevated levels of pyruvate and α-ketoglutarate in the blood  Arsenic poisoning kills PDH complex and α-ketoglutarate dehydrogenase, so you can’t make ATP! You die. Arsenite and mercury bind to sulfylhydryls of E3 coenzyme of PDH and α- ketoglutarate dehydrogenase. Thiol based chelators are great treatments for heavy atom poisoning. Ch 19: Harvesting Electrons from the Cycle  Function: complete oxidation of acetyl group from acetyl CoA to CO2 and transfer of electrons to form reducing equivalents NADH and FADH.  Who is Szent-Gyrogi? o Born in Hungary, WWI medic, Nobel Prize for vitamin C rxns in curing scurvy, part of the Hungarian resistance movement to oppose Nazism, established Institue for Muscle Research in Woods Hole, MA. o “fishes with a big hook” because it is more exciting to ask the big questions and not come up with anything than to only ask small questions and get small results.  Szent-Gyorgi experiment: if he added a small amount of oxaloacetate to his muscle suspensions, O2 consumption was 7x more than that needed for complete oxidation of the added oxaloacetate. Why does it stimulate O2 consumption and why is it so much greater than expected? o O2 consumption is an indication that CAC is functioning o When CAC intermediates are siphoned off for biosynthesis, any intermediate before it in the cycle and acetyl CoA accumulate. o When you add oxaloacetate, CAC can continue, and you burn through the excess oxaloacetate that accumulated  The CAC consists of 2 stages: 1) 2C introduced and released as CO2. Citrate is metabolized to a 4C molecule 2) The 4C molecule is metabolized to regenerate oxaloacetate *Does not include oxygen as a reactant and does not itself generate much ATP- it removes electrons from acetyl CoA and uses them to form NADH and FADH2 to power the electron transport chain, which makes ATP.  It is a cycle: must regenerate oxaloacetate. How do you regenerate oxaloacetate if you take something out of the cycle? You can convert pyruvate directly to oxaloacetate.  How would the CAC respond to an increase in NADH: inhibits enzymes and can only be oxidized in the mitochondria by ETC  Because this is an essential pathway, should an organism have an issue with their CAC the embryo wouldn’t even develop. Overall Reaction: Acetyl CoA + H 0  2CO +7H +8e + - 2 2  Fate of the Electrons- 6e go to 3 molecules of NAD - 2e go to 1 molecules of Q  Fate of the Protons- 3 protons to reduced NADH 2 protons to reduced QH 2  SO…… most of the energy released is conserved in the reduced coenzymes NADH and QH 2 Steps of the Citric Acid Cycle (pay most attention to energy-producing steps and regulating steps) 1) Citrate Synthase: Oxaloacetate reacts with acetyl CoA and H2O to yoeld citrate and CoA. a. The hydrlyolsis of the thioester (acetyl CoA) powers this synthesis and has a large - G b. Side reactions are minimized b/c oxaloacetate induces a major structural rearrangement when bound to citrate, leading to the creation of a binding site for acetyl CoA. “Induced fit” 2) Aconitase: Conversion of citrate to isocitrate. Equilibrium rxn. Stereospecific addition of H2O, resulting in dehydration/rehydration. Rearranges tertiary alcohol to secondary alcohol. 3) Isocitrate Dehydrogenase: Regulatory enzyme. First of 4 redox reactions in the CAC. a. *First production of NADH b. Reduction of NAD+, production of CO2, conversion of isocitrate to - ketoglutarate c. Allosterically stimulated by ADP- signified need for more energy d. Inhibited by NADH and ATP- signifies there is enough energy 4) -Ketoglutarate Dehydrogenase: regulated, rate-limiting step a. Analogous to pyruvate dehydrogenase complex (pyruvate  acetyl CoA) b. Produces NADH c. Inhibited by its products- succinyl CoA and NADH- as well as by ATP d. Assembly of 3 kinds of enzymes- E3 is exactly the same as PDH complex because the lipoamide needs to be regenerated, but the other 2 enzymes differ because the substrate is now -ketoglutarate, not pyruvate E1keto dehydrogenase (contains TPP) E2: dihydrolipoamide succinyl transferase (an FAD enzyme) E3: dihydrolipoamide dehydrogenase e. Both rxns include decarboxylation of an -ketoacid and subsequent formation of a thioester linkage with CoA. α-KDH couples the favorable oxidation of hydroxysuccinyl to the unfavorable succinylation of CoA End of Stage 1: 2 C have entered cycle, 2 C have been oxidized to CO2. The electrons from the oxidation have been captured in 2 molecules of NADH ---------------------------------------------------------------------------------------- Start of Stage 2: From now on the goal is to generate oxaloacetate 5) Succinyl- CoA Synthase: The hydrolysis of the high energy thioester bond of succinyl- CoA is coupled to the formation of GTP (or ATP). a. ONLY step in the citric acid cycle that directly yields a compound with a high phosphoryl-transfer potential (usually ATP) 6) Succinate Dehydrogenase Complex: Two subunits; one binds iron/sulfur clusters and the second binds FAD. a. Produces FADH2 b. It is bound to proteins in the inner mitochondrial membrane; has a Cyt B and a quinone binding site. FAD is the H acceptor in this rxn b/c the free energy chane is insufficient to reduce NAD+ c. Transfers 2 electrons directly from FADH2 to coenzyme Q, then The FADH is 2 oxidized back to FAD by Q. 7) Fumarase: Near equilibrium rxn. Forms trans-fumarate. a. Catalyzes the stereospecific addition of water to the double bond of fumarate 8) Malate Dehydrogenase: Oxidation of malate to oxaloacetate- coupled to the reduction of NAD- produces NADH a. Standard free energy for this step is positive, unlike any other step in the CAC, but the rxn is driven forward because the product, oxaloacetate, is being used up as soon as it’s formed- Le Chatelier’s principle Energy Producing steps of the cycle in red 2.5 molecules of ATP generated per molecule of NADH oxidized to NAD- (2.5 x 3) 1.5 molecules of ATP generated per molecule of QH ox2dized to Q- (1.5 x 1) 1 moleucle of ATP or GTP (1 x 1) 10 Lecture Question: If a person had white muscle tissue devoid of lactate dehydrogenase, how would this affect your metabolism in strenuous exercise? o Accumulation of NADH halts glycolysis. If you’re resting, you are undergoing aerobic reactions and don’t have this problem. Lecture Question: What are the functions of glycogen in the liver versus muscle? o Muscle: break it down to product Glc-6 phosphate for energy for glycolysis. Lacks enzyme that converts it back to glucose b/c muscles aren’t concerned with regulating blood glucose levels  Hexokinase has a lower Km (higher glucose affinity) and is inhibited by its product: can get saturated by Glc-6P and stop glycolysis o Liver: Regulate blood glucose levels. Broken down to glc-6 phosphate to be converted to glucose by enzyme  Glucokinase has a higher Km (lower glucose affinity) than hexokinase so glucose levels can never get high enough to saturate it. Allows the liver to make lots of Glc-6 phosphate. Never inhibited high levels of glucose, can handle high glucose levels after meals.


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