Question

The end product of purine catabolism in human is uric acid.

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True

False

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Question 691 pts

Gluconeogenesis takes place in the mitochondrion.

Group of answer choices

True

False

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Question 701 pts

The release of sn-diacylglycerol and inositol 1,4,5-triphosphate from phosphatidylinositol 4,5-bisphosphate is catalyzed by phospholipase A.

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True

False

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Question 711 pts

The net synthesis of oxaloacetate from acetyl CoA can occur via the TCA cycle.

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True

False

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Question 721 pts

Increase intracellular cAMP level in muscle can lead to increase fructose 2,6-bisphosphate level.

Group of answer choices

True

False

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Question 731 pts

A drastic increase in plasma triacylglycerols occurs during the early few days of starvation in humans.

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True

False

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Question 741 pts

The products of an aminotransferase-catalyzed reaction between pyruvate and glutamate would be alanine and a-ketoglutarate.

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True

False

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Question 751 pts

Agonists differ from antagonists in that only agonists can trigger intracellular metabolic changes.

Group of answer choices

True

False

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Question 761 pts

Ketone bodies are synthesized in mitochondria.

Group of answer choices

True

False

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Question 771 pts

Acetyl CoA does not provide the carbon skeletons for the biosynthesis of glucose.

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True

False

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Question 781 pts

Deoxyribonucleotides are formed by reduction of ribonucleoside diphosphates.

Group of answer choices

True

False

Answer 1

1) True. The end product of purine catabolism in man is uric acid. Other mammals have the enzyme urate oxidase and excrete the more soluble allantoin as the end product. Man does not have this enzyme so urate is the end product for us. Uric acid is formed primarily in the liver and excreted by the kidney into the urine.

Q691) True. The gluconeogenic pathway begins in the mitochondrion and ends in the cytoplasm.

Q701) False. The release of sn-diacylglycerol and inositol 1,4,5-triphosphate from phosphatidylinositol 4,5-bisphosphate is catalyzed by phospholipase C.

Q711) False. Citric acid cycle intermediates must be replenished if any are drawn off for biosyntheses. Suppose that much oxaloacetate is converted into amino acids for protein synthesis and, subsequently, the energy needs of the cell rise. The citric acid cycle will operate to a reduced extent unless new oxaloacetate is formed, because acetyl CoA cannot enter the cycle unless it condenses with oxaloacetate. Even though oxaloacetate is recycled, a minimal level must be maintained to allow the cycle to function. How is oxaloacetate replenished? Mammals lack the enzymes for the net conversion of acetyl CoA into oxaloacetate or any other citric acid cycle intermediate. Rather, oxaloacetate is formed by the carboxylation of pyruvate, in a reaction catalyzed by the biotin-dependent enzyme pyruvate carboxylase. This enzyme plays a crucial role in gluconeogenesis. It is active only in the presence of acetyl CoA, which signifies the need for more oxaloacetate. If the energy charge is high, oxaloacetate is converted into glucose. If the energy charge is low, oxaloacetate replenishes the citric acid cycle. The synthesis of oxaloacetate by the carboxylation of pyruvate is an example of an anaplerotic reaction, a reaction that leads to the net synthesis, or replenishment, of pathway components. As the citric acid cycle is a cycle, it can be replenished by the generation of any of the intermediates.

Q721) True. Increase intracellular cAMP level in muscle can lead to increase fructose 2,6-bisphosphate level.

Q731) True. A drastic increase in plasma triacylglycerols occurs during the early few days of starvation in humans. The metabolic changes on the first day of starvation are like those after an overnight fast. The low blood-sugar level leads to decreased secretion of insulin and increased secretion of glucagon. The dominant metabolic processes are the mobilization of triacylglycerols in adipose tissue and gluconeogenesis by the liver. The liver obtains energy for its own needs by oxidizing fatty acids released from adipose tissue. The concentrations of acetyl CoA and citrate consequently increase, which switches off glycolysis. The uptake of glucose by muscle is markedly diminished because of the low insulin level, whereas fatty acids enter freely. Consequently, muscle shifts almost entirely from glucose to fatty acids for fuel. The β-oxidation of fatty acids by muscle halts the conversion of pyruvate into acetyl CoA, because acetyl CoA stimulates the phosphorylation of the pyruvate dehydrogenase complex, which renders it inactive. Hence, pyruvate, lactate, and alanine are exported to the liver for conversion into glucose. Glycerol derived from the cleavage of triacylglycerols is another raw material for the synthesis of glucose by the liver.

Q741)True. When muscles degrade amino acids for energy needs, the resulting nitrogen is transaminated to pyruvate to form alanine. This is performed by the enzyme alanine transaminase (ALT), which converts L-glutamate and pyruvate into α-ketoglutarate and L-alanine.

Q751) True. Agonists differ from antagonists in that only agonists can trigger intracellular metabolic changes. Antagonists are molecules that bind the receptor and block binding of the agonist, but fail to trigger intracellular signalling events.

Q761) True. Ketone bodies are produced mainly in the mitochondria of liver cells, and synthesis can occur in response to an unavailability of blood glucose, such as during fasting.

Q771) True. Acetyl CoA does not provide the carbon skeletons for the biosynthesis of glucose. Amino acids that are degraded to acetyl CoA or acetoacetyl CoA are termed ketogenic amino acids because they can give rise to ketone bodies or fatty acids. Amino acids that are degraded to pyruvate, α-ketoglutarate, succinyl CoA, fumarate, or oxaloacetate are termed glucogenic amino acids. The net synthesis of glucose from these amino acids is feasible because these citric acid cycle intermediates and pyruvate can be converted into phosphoenolpyruvate and then into glucose.

Q781) True. Deoxyribonucleotides consist of a purine or a pyrimidine base bonded to deoxyribose, which in turn is bound to a phosphate group. They are synthesised by reduction of ribonucleoside diphosphates.