/hen the acetyl-CoA produced during B-oxidation in the liver exceeds the capacity of the citric acid ycle, the excess acetyl-CoA forms ketone bodies-acetone, acetoacetate, and D-b-hydroxybutyrate. This ccurs in severe, uncontrolled diabetes: because the tissues cannot use glucose, they oxidize large nounts of fatty acids instead. Although acetyl-CoA is not toxic, the mitochondrion must divert the cetyl-CoA to ketone bodies. What problem would arise if acetyl-CoA were not converted to ketone
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- Study Figure 19.18 and decide which of the following statements is false. Pyruvate dehydrogenase is inhibited by· NIADH. Pyruvate dehydrogenase is inhibited by AΤΡ. Citrate synthase is inhibited by NADH. Succinyl-CoA activates citrate synthase. Acetyl-CoA activates pyruvate carboxylase.When the acetyl-CoA produced during ß-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.
- B-oxidation of a 15:0 fatty acid will result in the production of O 7 acetyl CoA, 7 FADH2, and 7 NADH O 7 acetyl CoA, 1 propionyl CoA, 8 FADH2, and 8 NADH 6 acetyl CoA, 1 propionyl CoA, 7 FADH2, and 7 NADH 6 acetyl CoA, 1 propionyl CoA, 6 FADH2, and 6 NADH. Glucagon secretion causes inhibition of intracellular acetyl-CoA car- boxylase activity by several mechanisms. Name all you can think of.Consider the docosanoic acid, C21H43CO2H a. Label the a and B carbons b. Draw the acyl CoA derived from this fatty acid c. How many acetyl CoA molecules are formed by complete B-oxidation? d. How many cycles of B-oxidation are needed for complete oxidation? e. How many molecules of ATP are formed from the complete catabolism of this fatty acid?
- 10. The patients with a genetically determined medium-chain acyl-CoA dehydrogenase (MCAD) deficiency suffer from episodes of profound fatigue associated with vomiting, which is happening if they fasted for more than 8 hours. They have hypoglycemia, clevated level of free fatty acids in the blood but ketone bodies were below normal. Explain the development of these symptoms. For that answer the question and do the following tasks: a) why hypoglycemia occurs in the patients fasting for more than 8 hours? b) why the level of free fatty acids is elevated in blood? Write the scheme explaining this symptom; c) draw the scheme of fatty acid metabolism, which is blocked in case of this genetic disorder.7) What are the major pathways of glucose utilizations that are vary with physiological conditions, and organisms? (Describe the three possible fates of pyruvate) .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.
- Glucagon secretion inhibits intracellular acetyl-CoA carboxylase activity through a number of different methods. Make a list of everything that comes to mind.2. (a) ( In contrast to the pyruvate dehydrogen- ase complex, the a-ketoglutarate dehydrogenase (aKGDH) complex is not up- or downregulated by phosphorylation or dephosphorylation. However, the complex exhibits cooperativity modulated by the presence of ADP, ATP, inorganic phosphate (Pi), and Ca2+, as illustrated by the diagram on the right for the bovine kidney enzyme complex. Note in the diagram how the addition of 10 μM Ca2+ shifts the affinity of the enzyme complex for aKG from 20 mM Pi/-Ca2+ to 20 mM Pi/+Ca2+. Calcium especially en- hances the cooperative influence of ADP and ATP. Using the expanded copy of the diagram at the end of the problem set, estimate the change in S0.5 (re- member that for allosteric enzymes S0.5 corresponds to KM of a nonallosteric enzyme) for the enzyme complex in the presence of 20 mM Pi/-Ca2+ and in the presence of 20 mM Pi/+Ca2+. Compare similarly the change in S0.5 for the enzyme in the presence of 20 mM Pi/-Ca2+ plus 1.6 mM ADP to the enzyme in the…1. Fatty acids are transported into the mitochondria as fatty acyl-carnitine rather than fatty acyl-CoA and B-hydroxybuturate and acetoacetate (ketone bodies) are exported out of the liver into the blood rather than their -CoA esters. Why?