Which of the following is NOT a metabolic fate of pyruvate? The pyruvate dehydrogenase complex catalyzes the oxidative decarboxylation of pyruvate to form acetyl-CoA. Pyruvate carboxylase catalyzes the carboxylation of pyruvate to form oxaloacetate. Pyruvate kinase catalyzes the formation of phosphoenolpyruvate from pyruvate. Lactate dehydrogenase catalyzes the formation of lactate from pyruvate.
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Which of the following is NOT a
- The pyruvate dehydrogenase complex catalyzes the oxidative decarboxylation of pyruvate to form acetyl-CoA.
- Pyruvate carboxylase catalyzes the carboxylation of pyruvate to form oxaloacetate.
- Pyruvate kinase catalyzes the formation of phosphoenolpyruvate from pyruvate.
- Lactate dehydrogenase catalyzes the formation of lactate from pyruvate.
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- Which of the following is most likely to cause accumulation of acetyl CoA? Group of answer choices There is not enough oxaloacetate present to run the citric acid cycle Increase activity of pyruvate dehydrogenase kinase Increased fatty acid synthesis Increased citrate synthase activity When fluoroacetate (an analog of acetate) is added to the mitochondria, it causes build up of fluorocitrate. Which of the following is most likely to be true? Group of answer choices Fluoroacetate cannot be converted to fluoroacetyl CoA Fluoroacetyl CoA cannot be combined with oxaloacetate to enter the citric acid cycle Addition of fluoroacetate will cause an increase in isocitrate Aconitase cannot use fluorocitrate as a substrateThe pyruvate dehydrogenase (PDH) complex catalyzes the oxidative decarboxylation of pyruvate to acetyl‑CoA and CO2.CO2. Multiple copies of pyruvate dehydrogenase (E1), dihydrolipoyl transacetylase (E2), and dihydrolipoyl dehydrogenase (E3) along with five cofactors form the PDH complex. Biochemists have studied the PDH complex for decades, in part due to its interesting use of substrate channeling during catalysis. What is the molecular mechanism of substrate channeling in the PDH complex? A. The swinging lipoyllysyl arm of E2 carries electrons and an acetyl group from E1 to E2. B.The active sites of E1, E2, and E3 undergo conformational changes that move products of one reaction to their next position without solvent exposure. C.Electrons and an acetyl group travel between E1 and E2 through a tunnel in E2. D. Metal ions coordinated with thiamine pyrophosphate (TPP) in E1 shield the electrons and acetyl group from scavenging by other enzymes until they reach E3.The pyruvate dehydrogenase (PDH) complex catalyzes the oxidative decarboxylation of pyruvate to acetyl‑CoA and CO2.CO2. Multiple copies of pyruvate dehydrogenase (E1), dihydrolipoyl transacetylase (E2), and dihydrolipoyl dehydrogenase (E3) along with five cofactors form the PDH complex. Biochemists have studied the PDH complex for decades, in part due to its interesting use of substrate channeling during catalysis. What is the benefit of substrate channeling? A. Intermediates of a multistep reaction sequence do not dissociate from the enzyme complex. B. Every intermediate or product made by the PDH complex enters the citric acid cycle as a substrate. C. The PDH complex sequesters excess substrate to use at later time. D. Reaction progress is not limited by the diffusion constant. E.The PDH active site forms in the hydrophobic core of the complex instead of a surface‑exposed region.
- Pyruvate can be converted to glucose via gluconeogenesis, or it can be oxidized to acetyl-CoA for energy production. The enzyme pyruvate carboxylase is regulated allosterically by which of the following? Oxaloacetate All of the above Acetyl COA Glucose-6-phosphate Fructose-6-phosphateElevated levels of acetyl-CoA will act as an effector for which of the following enzymes? Pyruvate carboxylase. Pyruvate kinase Pyruvate dehydrogenase. Citrate synthase a-Ketoglutarate dehydrogenase.Elevated levels of acetyl-CoA will act as an effector for which of the following enzymes? more than one can be correct Pyruvate carboxylase. Pyruvate kinase Pyruvate dehydrogenase. Citrate synthase a-Ketoglutarate dehydrogenase.
- A fatty acid (a long straight-chain carboxylic acid with an even number of carbons) is metabolized to acetylCoA, which can then enter the citric acid cycle to be further metabolized. A fatty acid with an odd number of carbons is metabolized to acetyl-CoA and one equivalent of propionyl-CoA. Propionyl-CoA cannot enter the citric acid cycle. Two coenzyme-requiring enzymes are needed to convert it to succinyl-CoA, a compound that can enter the citric acid cycle. Write the two enzyme-catalyzed reactions and include the names of the required coenzymes.Which one of the following statements about PEP (phosphoenolpyruvate) synthesis is correct? Pyruvate can be converted to PEP by a combination of reactions that use energy from two different types of nucleotide triphosphate Pyruvate can be converted to PEP by pyruvate kinase via a single reaction. Pyruvate can be converted to PEP by a mutase. Pyruvate is converted to PEP by the citric acid cycle.Which of the following is an important enzyme involved in the synthesis of cholesterol from isoprene pyrophosphate? thiolase pyruvate decarboxylase pyruvate dehydrogenase HMG-CoA reductase glucose oxidase
- Which of the following glycolytic enzymes catalyzes the conversion of fructose-1,6-bisphosphate into the two product molecules dihydroxyacetone phosphate, and glyceraldehyde-3-phosphate? phosphoglycerate kinase pyruvate kinase malate dehydrogenase aldolase phosphofructokinaseWhen the acetyl-CoA produced during B-oxidation in the liver exceeds the capacity of the citric acid cycle, the excess acetyl-CoA forms ketone bodies-acetone, acetoacetate, and D-b-hydroxybutyrate. This occurs in severe, uncontrolled diabetes: because the tissues cannot use glucose, they oxidize large amounts of fatty acids instead. Although acetyl-CoA is not toxic, the mitochondrion must divert the acetyl-CoA to ketone bodies. What problem would arise if acetyl-CoA were not converted to ketone bodies? How does the diversion to ketone bodies solve the problem?When the acetyl-CoA produced during ß-oxidation in the liver exceeds the capacity of the citric acid cycle, the excess acetyl-CoA forms ketone bodies acetone, acetoacetate, and D-b-hydroxybutyrate. This occurs in severe, uncontrolled diabetes: because the tissues cannot use glucose, they oxidize large amounts of fatty acids instead. Although acetyl-CoA is not toxic, the mitochondrion must divert the acetyl-CoA to ketone bodies. What problem would arise if acetyl-CoA were not converted to ketone bodies? How does the diversion to ketone bodies solve the problem?