When the acetyl-CoA produced during ß-oxidation in the liver exceeds the capacity of the citric acidcycle, the excess acetyl-CoA forms ketone bodies acetone, acetoacetate, and D-b-hydroxybutyrate. Thisoccurs in severe, uncontrolled diabetes: because the tissues cannot use glucose, they oxidize largeamounts of fatty acids instead. Although acetyl-CoA is not toxic, the mitochondrion must divert theacetyl-CoA to ketone bodies. What problem would arise if acetyl-CoA were not converted to ketonebodies? How does the diversion to ketone bodies solve the problem?

When there is an accumulation of acetyl CoA in the cell due to excessive beta-oxidation, ketone…

Answered: When the acetyl-CoA produced during…

Biochemistry

6th Edition

ISBN:9781305577206

Author:Reginald H. Garrett, Charles M. Grisham

Publisher:Reginald H. Garrett, Charles M. Grisham

Chapter19: The Tricarboxylic Acid Cycle

Section: Chapter Questions

Problem 22P: Study Figure 19.18 and decide which of the following statements is false. Pyruvate dehydrogenase is...

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When the acetyl-CoA produced during B-oxidation in the liver exceeds the capacity of the citric acid cycle, the excess acetyl-CoA forms ketone bodies-acetone, acetoacetate, and D-b-hydroxybutyrate. This occurs in severe, uncontrolled diabetes: because the tissues cannot use glucose, they oxidize large amounts of fatty acids instead. Although acetyl-CoA is not toxic, the mitochondrion must divert the acetyl-CoA to ketone bodies. What problem would arise if acetyl-CoA were not converted to ketone bodies? How does the diversion to ketone bodies solve the problem?
In type I diabetes mellitus, excessive production of acetyl-CoA may surpass the body’s capacity to oxidize it. As a result, acetoacetate, β-hydroxybutyrate, and acetone (ketone bodies) accumulate. When generated in large amounts, blood pH falls, thereby reducing the capacity of red blood cells to carry oxygen. Explain in general terms how high concentrations of ketone bodies may result in a fatal coma.
In the presence of saturating amounts of oxaloacetate, the activity of citrate synthase from pig heart tissue shows a sigmoid dependence on the concentration of acetyl‑CoA. When succinyl‑CoA is added, the curve shifts to the right and the sigmoid dependence is more pronounced.
Pyruvate dehydrogenase deficiency is a fatal disease usually diagnosed in children. Symptoms include severe neurological damage. Elevated blood levels of lactate, pyruvate, and alanine are also seen. Explain how the deficiency of pyruvate dehydrogenase causes these elevated values.
One of the consequences of ethanol addiction is fattyliver disease, an illness in which liver cells accumulatetriacylglycerols, the esters derived from glycerol and fattyacids. Ethanol is oxidized in the cytoplasm of liver cells byalcohol dehydrogenase and aldehyde dehydrogenase to yieldacetate and 2 NADH. Acetate is then transported into themitochondrion, where it is converted to acetyl-CoA andmetabolized by the citric acid cycle. When alcohol is consumed in excessive quantities, the resulting high levels ofNADH cause metabolic abnormalities, one of which is highlevels of fatty acid synthesis. Fatty acid synthesis, also acytoplasmic process, uses acetyl-CoA as a substrate andNADPH as a reducing agent. Determine how a high level ofcytoplasmic NADH provides a source of NADPH for fattyacid synthesis.
Fatty acid biosynthesis begins with the condensation of a two-carbon acetyl residue from acetyl-COA and oxaloacetate, while oxidation leads to the release of two carbon units, acetyl-CoA and fatty acyl-CoA. However, these two processes are not simple reversal. Compare and contrast these two pathways.
Glucagon secretion causes inhibition of intracellular acetyl-CoA carboxylase activity by several mechanisms. Name all you can think of.
Which of the following fatty acids will produce propionyl-CoA in its/their last β-oxidation cycle?
The diabetic body's reliance on ketogenesis to provide energy due to the unavailability of glucose causes serious health and toxicity concerns in these individuals. 1) Describe the role of ketogenesis in diabetes, why the body elects this metabolic pathway, and its resultant benefits and consequences. 2) Describe the role of ketogenesis in a ketogenic diet, why this can be considered a desired metabolic state for individuals, and the benefits and consequences of ketogenesis in these intentional circumstances. Rationalize the differences between these two ketogenic instances.
After several days of starvation, the capacity of the liver to metabolize acetyl-CoA via the citric acid cycle is greatly diminished. Explain.
A number of genetic deficiencies in acyl CoA dehydrogenases have been described. This deficiency presents early in life after a period of fasting. Symptoms include vomiting, lethargy, and sometimes coma. Not only are blood levels of glucose low ( hypoglycemia), but starvation-induced ketosis is absent. Provide a biochemical explanation for these last two observations.
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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