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An individual developed a condition characterized by progressive muscular weakness and aching muscle cramps. Fasting. exercise, and a high-fat diet aggravated the symptoms. The homogenate of a skeletal muscle specimen from the patient oxidized added oleate more skowly than did control homogenates consisting of muscle specimens from healthy individuals. When the pathologist added carnitine to the patient's muscle homogenate, the rate of oleate oxidation equaled that in the control homogenates. Based on these results, the attending physician diagnosed the patient as having a carnitine deficiency. Why did added carnitine increase the rate of oleate oxidation in the patient's muscle homogenate? The carnitine shuttle transports coenzyme A across the mitochondrial membrane to aid in fatty acid oxidation. Carnitine is a required cofactor for the fatty acid oxidation enzyme acyl-CoA dehydrogenase. The carnitine-mediated entry of fatty acids into mitochondria is the rate-limiting step in fatty acid oxidation. Carnitine is a citric acid cycle intermediate and, without it, acetyl-CoA builds up, inhibiting fatty acid oxidation Why did fasting, exercise, and a high-fat diet aggravate the paticat's symptoms?

An individual developed a condition characterized by progressive muscular weakness and aching muscle cramps. Fasting. exercise, and a high-fat diet aggravated the symptoms. The homogenate of a skeletal muscle specimen from the patient oxidized added oleate more skowly than did control homogenates consisting of muscle specimens from healthy individuals. When the pathologist added carnitine to the patient's muscle homogenate, the rate of oleate oxidation equaled that in the control homogenates. Based on these results, the attending physician diagnosed the patient as having a carnitine deficiency. Why did added carnitine increase the rate of oleate oxidation in the patient's muscle homogenate? The carnitine shuttle transports coenzyme A across the mitochondrial membrane to aid in fatty acid oxidation. Carnitine is a required cofactor for the fatty acid oxidation enzyme acyl-CoA dehydrogenase. The carnitine-mediated entry of fatty acids into mitochondria is the rate-limiting step in fatty acid oxidation. Carnitine is a citric acid cycle intermediate and, without it, acetyl-CoA builds up, inhibiting fatty acid oxidation Why did fasting, exercise, and a high-fat diet aggravate the paticat's symptoms?

Biochemistry
Biochemistry
9th Edition
ISBN:9781319114671
Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.
Publisher:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.
Chapter1: Biochemistry: An Evolving Science
Section: Chapter Questions
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An individual developed a condition characterized by progressive muscular weakness and aching muscle cramps. Fasting. exercise, and a hiyh-fat diet aggravated the symptoms. The homogenate of a skeletal muscle specimen from the patient oxidized added oleate more slowly than did control homogenates consisting of muscle specimens from healthy individuals. When the pathologist added carnitine to the patient's muscle homogenate, the rate of oleate oxidation equaled that in the control homogenates. Based on these results, the attending physician diagnosed the patient as having a carnitine deficiency. Why did added carnitine increase the rate of oleate oxidation in the patient's muscle homogenate? The carnitine shuttle transports coenzyme A across the mitochondrial membrane to aid in fatty acid oxidation. Carnitine is a required cofactor for the fatty acid oxidation enzyme acyl-CoA dehydrogenase. The carnitine-mediated entry of fatty acids into mitochondria is the rate-limiting step in fatty acid oxidation. Carnitine is a citric acid cycle intermediate and, without it, acetyl-CoA builds up, inhibiting fatty acid oxidation. Why did fasting, exercise, and a high-fat diet aggravate the patient's symptoms?
Transcribed Image Text:An individual developed a condition characterized by progressive muscular weakness and aching muscle cramps. Fasting. exercise, and a hiyh-fat diet aggravated the symptoms. The homogenate of a skeletal muscle specimen from the patient oxidized added oleate more slowly than did control homogenates consisting of muscle specimens from healthy individuals. When the pathologist added carnitine to the patient's muscle homogenate, the rate of oleate oxidation equaled that in the control homogenates. Based on these results, the attending physician diagnosed the patient as having a carnitine deficiency. Why did added carnitine increase the rate of oleate oxidation in the patient's muscle homogenate? The carnitine shuttle transports coenzyme A across the mitochondrial membrane to aid in fatty acid oxidation. Carnitine is a required cofactor for the fatty acid oxidation enzyme acyl-CoA dehydrogenase. The carnitine-mediated entry of fatty acids into mitochondria is the rate-limiting step in fatty acid oxidation. Carnitine is a citric acid cycle intermediate and, without it, acetyl-CoA builds up, inhibiting fatty acid oxidation. Why did fasting, exercise, and a high-fat diet aggravate the patient's symptoms?
Carnitine is a citric acid cycle intermediate and, without it, acetyl-CoA builds up, inhibiting fatty acid oxidation. Why did fasting., exercise, and a high-fat diet aggravate the patient's symptoms? Insulin levels in the blood increased. The metabolic need for fatty acid oxidation increased. The demand for ketogenesis decreased. The rate of glycolysis increased. Select the possible reasons for the deficiency of muscle carnitine in this individual. O high levels of ATP, an inhibitor of fatty acid synthesis a deficiency of a carnitine precursor such as lysine a defect in one of the enzymes in the biosynthesis of carnitine Olow levels of tetrahydrofolate, a cofactor in carnitine biosynthesis please explain before giving answer and answer all
Transcribed Image Text:Carnitine is a citric acid cycle intermediate and, without it, acetyl-CoA builds up, inhibiting fatty acid oxidation. Why did fasting., exercise, and a high-fat diet aggravate the patient's symptoms? Insulin levels in the blood increased. The metabolic need for fatty acid oxidation increased. The demand for ketogenesis decreased. The rate of glycolysis increased. Select the possible reasons for the deficiency of muscle carnitine in this individual. O high levels of ATP, an inhibitor of fatty acid synthesis a deficiency of a carnitine precursor such as lysine a defect in one of the enzymes in the biosynthesis of carnitine Olow levels of tetrahydrofolate, a cofactor in carnitine biosynthesis please explain before giving answer and answer all
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