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All of the following statements about acetyl-CoA carboxylase are correct except A. it catalyzes the rate-limiting step of fatty acid synthesis. B. it requires biotin. C. it is inhibited by cAMP-mediated phosphorylation. D. it is activated by palmitoyl CoA. E. its content in a cell responds to changes in fat content in the diet.

Short Answer

Expert verified
Answer: D. Acetyl-CoA carboxylase is activated by palmitoyl CoA.

Step by step solution

01

Statement A

Acetyl-CoA carboxylase catalyzes the rate-limiting step of fatty acid synthesis. This statement is correct. Acetyl-CoA carboxylase converts acetyl-CoA to malonyl-CoA, which is the rate-limiting step in fatty acid synthesis.
02

Statement B

Acetyl-CoA carboxylase requires biotin. This statement is also correct. Biotin is a coenzyme that is essential for the carboxylation reaction performed by acetyl-CoA carboxylase.
03

Statement C

Acetyl-CoA carboxylase is inhibited by cAMP-mediated phosphorylation. This statement is correct as well. The enzyme is regulated by both allosteric factors and covalent modification through phosphorylation, which is mediated by the cAMP-activated protein kinase A.
04

Statement D

Acetyl-CoA carboxylase is activated by palmitoyl CoA. This statement is incorrect. In fact, the enzyme is inhibited by palmitoyl CoA, a long-chain fatty acyl-CoA, which reflects that when the products of the fatty acid synthesis pathway are abundant, the enzyme is downregulated to prevent excessive synthesis.
05

Statement E

Acetyl-CoA carboxylase content in a cell responds to changes in fat content in the diet. This statement is correct. The enzyme is regulated at both the transcriptional and post-translational levels, and the content of the enzyme in a cell is influenced by nutritional factors and hormones. Based on the analysis of each statement, the incorrect statement about acetyl-CoA carboxylase is: D. Acetyl-CoA carboxylase is activated by palmitoyl CoA.

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Most popular questions from this chapter

\(\alpha\) -Oxidation A. is important in the metabolism of branched chain fatty acids. B. metabolizes a fatty acid completely to acetyl CoA. C. produces hydrogen peroxide. D. prevents the fatty acid from producing energy. E. requires NADPH.

One of the problems associated with obesity is the increased risk of Type 2 diabetes. High fatty acid concentration in the blood reduces glucose uptake and metabolism by skeletal muscle, increasing levels of blood glucose and insulin secretion (insulin resistance). Prolonged overproduction of insulin can cause failure of the \(\beta\) cells of the pancreas and Type 2 diabetes. This occurs in \(\sim 40 \%\) of obese individuals over \(5-10\) years. One way of regulating the concentration of fatty acids in blood is their reesterification into triacylglycerols. One type of antidiabetic drug (thiazolidinedione) acts on a nuclear receptor (PPAR \(\gamma 2\) ) facilitating the rate of fatty acid esterification in white adipose tissue. All of the following events are usually involved in the synthesis of triacylglycerols in adipose tissue except A. addition of a fatty acyl CoA to a diacylglycerol. B. addition of a fatty acyl CoA to a lysophosphatide. C. a reaction catalyzed by glycerol kinase. D. hydrolysis of phosphatidic acid by a phosphatase. E. reduction of dihydroxyacetone phosphate.

Medium-chain acyl-CoA dehydrogenase deficiency \((\mathrm{MCAD}),\) a defect in \(\beta\) -oxidation, usually produces symptoms within the first 2 years of life after a period of fasting. Typical symptoms include vomiting, lethargy, and hypoketotic hypoglycemia. Excessive urinary secretion of medium-chain dicarboxylic acids and medium-chain esters of glycine and carnitine help to establish the diagnosis. The lack of ketone bodies in the presence of low blood glucose in this case is unusual since ketone body concentrations usually increase with fasting-induced hypoglycemia. Ketone bodies A. are formed by removal of CoA from the corresponding intermediate of \(\beta\) -oxidation. B. are synthesized from cytoplasmic \(\beta\) -hydroxy- \(\beta\) -methyl glutaryl coenzyme \(A(\mathrm{H} \mathrm{MG}-\mathrm{CoA})\) C. are synthesized primarily in muscle tissue. D. include both \(\beta\) -hydroxybutyrate and acetoacetate, the ratio reflecting the intramitochondrial [NADH]/[NAD \(\left.^{+}\right]\) ratio in liver. E. form when \(\beta\) -oxidation is interrupted.

One of the problems associated with obesity is the increased risk of Type 2 diabetes. High fatty acid concentration in the blood reduces glucose uptake and metabolism by skeletal muscle, increasing levels of blood glucose and insulin secretion (insulin resistance). Prolonged overproduction of insulin can cause failure of the \(\beta\) cells of the pancreas and Type 2 diabetes. This occurs in \(\sim 40 \%\) of obese individuals over \(5-10\) years. One way of regulating the concentration of fatty acids in blood is their reesterification into triacylglycerols. One type of antidiabetic drug (thiazolidinedione) acts on a nuclear receptor (PPAR \(\gamma 2\) ) facilitating the rate of fatty acid esterification in white adipose tissue. Glycerol-3-phosphate for triacylglycerol synthesis A. is always formed by reduction of dihydroxyacetone phosphate. B. can be formed in liver by glyceroneogenesis but not in adipose tissue. C. derives its carbons primarily from amino acids in the fed state. D. can be synthesized only in the presence of phosphoenolpyruvate carboxykinase. E. is derived primarily from glucose via glycolysis in the fed state.

Following a severe cold which caused a loss of appetite, a 1 -year-old boy was hospitalized with hypoglycemia, hyperammonemia, muscle weakness, and cardiac irregularities. These symptoms were consistent with a defect in the carnitine transport system. Dietary carnitine therapy was tried unsuccessfully, but a diet low in long-chain fatty acids and supplemented with medium-chain triacylglycerols was beneficial. Carnitine transport of fatty acids from the cytosol to the mitochondria involves all of the following except A. hydrolysis of ATP. B. the exchange of acylcarnitine and free carnitine across the inner mitochondrial membrane. C. two carnitine palmitoyl transferases (CPT I and CPT II) located on different mitochondrial membranes. D. release of CoASH from fatty acyl CoA in the cytosol. E. consumption of mitochondrial CoASH.

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