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Chapter 17: Problem 3

In humans, desaturation of fatty acids A. occurs primarily in mitochondria. B. is catalyzed by an enzyme system that uses NADPH and a cytochrome. C. introduces double bonds primarily of trans configuration. D. can occur only after palmitate has been elongated to stearic acid. E. introduces the first double bond at the methyl end of the molecule.

Short Answer

Expert verified
Answer: Desaturation of fatty acids in humans is catalyzed by an enzyme system that uses NADPH and a cytochrome.

Step by step solution

01

Option A: Occurs primarily in mitochondria

This is not correct. While fatty acid oxidation and synthesis occur in the mitochondria, desaturation takes place primarily in the endoplasmic reticulum.
02

Option B: Is catalyzed by an enzyme system that uses NADPH and a cytochrome

This is correct. The enzyme system involved in desaturation is called fatty acid desaturase. This enzyme system utilizes NADPH and a cytochrome as coenzymes to introduce double bonds into the fatty acid chains.
03

Option C: Introduces double bonds primarily of trans configuration

This is not correct. In human desaturation, the introduced double bonds are of the cis configuration.
04

Option D: Can occur only after palmitate has been elongated to stearic acid

This is not correct. Desaturation can occur at various chain lengths, not only after the conversion of palmitate to stearic acid.
05

Option E: Introduces the first double bond at the methyl end of the molecule

This is not correct. Desaturation introduces double bonds starting from the carboxyl end of the fatty acid molecule, not the methyl end. Based on the analysis, the correct answer is: B. Desaturation of fatty acids in humans is catalyzed by an enzyme system that uses NADPH and a cytochrome.

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Most popular questions from this chapter

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.

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.

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. 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.
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