The symptoms shown in a patient with carnitine-deficiency are normally muscular weaknessand muscle cramps. In an experiment, the homogenates of the skeletal muscle specimen fromhealthy individuals and carnitine-deficient patient were used to oxidize a fatty acid and theirrates of oxidation were compared.(i)What do you think will be the rates of oxidation of the fatty acid by the twosamples of homogenates? Explain your results by referring to the role of carnitine infatty acid oxidation.(ii)Explain why the patient's symptoms worsen with starvation.

Fatty acyl co A formed in the outer mitochondrial membrane do not cross the inner mitochondrial…

Answered: healthy individuals and…

Human Anatomy & Physiology (11th Edition)

11th Edition

ISBN:9780134580999

Author:Elaine N. Marieb, Katja N. Hoehn

Publisher:Elaine N. Marieb, Katja N. Hoehn

Chapter1: The Human Body: An Orientation

Section: Chapter Questions

Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...

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Similar questions

What structurtal property of mono- and polyunsaturated fatty acids prevents oxidation of these compounds by the β-oxidation pathway? what additional types of reactions are needed?
Adults who participate in vigourous physical exercise need around 160 g of carbohydrate per day but just approximately 20 mg of niacin for good nutrition. How do you interpret the finding in light of niacin's involvement in glycolysis?
We have stated that fatty acids cannot yield a net gain in carbohydrates in organisms that lack a glyoxalate pathway. Why can odd-chain fatty acids be thought to break this rule to a small extent?
In considering the carbohydrate maltose... a. How many molecules of acetyl CoA are formed from its complete catabolism? b. How many rounds of Citric acid Cycle must occur to complete catabolism? c. How many rounds of electron transport chain and oxidative phosphorylation?
Can the carbons in ketones be metabolized and wind up in a glucose monosaccharide? If yes, using merely the information presented in class, outline a possible metabolic route for these carbons. If no, explain why not.
In the liver, fructose can be converted into glyceraldehyde 3- phosphate and dihydroxyacetone phosphate without passing through the phosphofructokinase-regulated reaction. Show the reactions that make this conversion possible. Why might ingesting high levels of fructose have deleterious physiological effects?
What is the total energetics involved in the complete beta-oxidation of one mole of 19C fatty acid including the indication of the number of cycles and the number of acetylCoA produced and also the number of ATPs used and indicate clearly these reactions which are important for the generation of ATP?
Although animals cannot synthesize glucose from acetyl-CoA, if a rat is fed 14C-labeled acetate, some of the label appears in glycogen extracted from its muscles. Explain.
Can the fatty acid B be used to generate glucose in animals and is this possible for an unbranched 8-carbon fatty acid as well?
Considering the complete oxidation of an 18-C fatty acid. Give the answer for the following question.a. How many rounds of beta-oxidation is needed?b. How many NADH molecules are produced in beta-oxidation only?c. How many FADH2 molecules are produced in beta-oxidation only?d. How many Acetyl Co-A are produced?
Considering that triacylglycerols get hydrolyzed in the small intestine because of pancreatic lipases, write the reactions using structural formulas by which a 7-carbon fatty acid is activated and oxidized in the liver of this patient. Indicate cofactors and underscore the final CoA products.
How does the yield of ATP from complete oxidation of onemolecule of glucose in muscle and brain differ from that in liver,heart, and kidney? What is the underlying reason for this difference?

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