
Biochemistry
6th Edition
ISBN: 9781305577206
Author: Reginald H. Garrett, Charles M. Grisham
Publisher: Cengage Learning
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Question
What is the difference between?
HMG CoA in cholesterol biosynthesis and in
Citrate shuttle and carnitine shuttle
Type I familial hyperchylomicronemia and Type II A hypercholesterolemia
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Complete oxidation of a 16-carbon fatty acid can yield 129 molecules of ATP Study Figure 19.2 and determine how many ATP molecules would be generated if a 16-carbon fatly acid were metabolized solely by the TCA cycle, in the form of S acetyl-CoA molecules.
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GTP or ATP is produced during the conversion of isocitrate into ketoglutarate succinyl CoA into succinate fumarate into malate malate into oxaloacetate
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Acetyl CoA can be converted to all of the following except ________. ketone bodies fatty acids polysaccharides triglycerides
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What is the rate-limiting step in the synthesis of acetyl CoA?
oxidation
regeneration of lipoamide
decarboxylation
transfer to lipoamide
transfer to CoA
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Glucagon secretion inhibits intracellular acetyl-CoA carboxylase activity through a number of different methods. Make a list of everything that comes to mind.
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True or false
1. During fatty acid biosynthesis, acetyl CoA is the donor of the acetyl group.
2. Pyruvate serves as the precursor of the glycerol backbone during TAG biosynthesis.
3. Malonyl CoA is an inhibitor of acetyl CoA carboxylase.
4. HMG-CoA serves as the common intermediate of cholesterol biosynthesis and ketogenesis.
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The number of CO2 molecules liberated for each molecule of acetyl-CoA during oxidative decarboxylation reactions in TCA cycle.
The number of steps in gluconeogenesis that are the reverse of glycolytic reactions.
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The acyl-CoA dehydrogenase deficiency diseases are a groupof inherited defects that impair the b-oxidation of fatty acids.Symptoms of the disease range from nausea and vomiting tofrequent comas. Symptoms may be alleviated by eating regularly and avoiding periods of starvation (12 hours or more).Why does this simple procedure alleviate the symptoms?
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A patient exhibiting all the symptoms of beriberi is placed on a thiamine-enriched diet; however, the symptoms do not disappear. Genetic screening suggests a defect in pyruvate dehydrogenase phosphatase. Briefly explain why the genetic defect caused beriberi symptoms andy why thiamine supplementation had no effect.
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Malonyl-CoA synthesized by the action of acetyl-CoA carboxylase II is primarily used:a. To synthesize fatty acidsb. To inhibit fatty acid oxidationc. Both a and bd. Neither a nor b
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Two siblings born years apart were separately diagnosed with pyruvate carboxylase deficiency. Both neonates died less than a month after they were born. Blood samples taken before the death of the infants showed a high concentration of ketone bodies in the blood. Explain why the ketone body concentration was elevated.
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Name three enzymes and/or genes that you will evaluate in order to verify increased de novo lipogenesis in adipose tissue in response to CHO overfeeding and explain why pentose phosphate pathway may be important for this process.
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