In own words, give 5 or more reasons why most of the clinical features of the diseases a-ketoglutarate dehydrogenase deficiency, succinate dehydrogenase deficiency, and fumarase deficiency involve muscle and nerve tissue? and explain those reasons.
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In own words, give 5 or more reasons why most of the clinical features of the diseases a-ketoglutarate dehydrogenase deficiency, succinate dehydrogenase deficiency, and fumarase deficiency involve muscle and nerve tissue? and explain those reasons.
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- Why most of the clinical features of the diseases Krebs Cycle inborn errors ( a- ketoglutarate dehydrogenase deficiency, succinate dehydrogenase deficiency, and fumarase deficiency) involve muscle and nerve tissue?What are the diseases a-ketoglutarate dehydrogenase deficiency, succinate dehydrogenase deficiency, and fumarase deficiency? and why most of these disease clinical features of these diseases involve muscle and nerve tissue?In your own words, what do you think is/are the reason/s why most of the clinical features of these diseases involve muscle and nerve tissue(Deficiencies of a-KG dehydrogenase, succinate de-hydrogenase SDH and fumarase?
- 10a) Outline the mechanism for the conversion of alpha-ketoglutarate to succinyl-CoA which is catalyzed by alpha-ketoglutarate dehydrogenase. b) Of the five steps involved with this process, which would most likely be metabolically irreversible under physiological conditions?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.Von Gierke’s disease is a rare genetic disorder that results in a deficiency of glucose-6-phosphatase. Symptoms ketoacidosis, a buildup of glycogen in the liver, and lactate buildup. Why does this glycogen storage disease not affect the brain? a) The brain is able to still perform glycolysis effectively b) None of the above c) In the event of hypoglycemia, the brain is able to utilize other sources of energy to produce ATP d) The brain is able to metabolize lactate, which is present in high concetrations.
- What are the effects of Glucose-6 Phosphate Dehydrogenase Deficiency? Explain its mechanism of action.Describe one mechanism that leads to continued gluconeogenesis in the liver of T1DM patients, despite already high levels of glucose in the bloodstream.The aminoacids, phenylalanine and tyrosine, are degraded to acetoac- etate and fumarate by a single pathway. Name the diseases related to this pathway.
- How can these deficiencies (a-KG dehydrogenase, Succinate dehydrogenase (SDH), Fumarase) negatively impact the function of cells, tissues and organs in the body? Explain.Refer to Figure, which indicates ΔG for each glycolytic reaction under intracellular conditions. Assume that glyceraldehyde-3-phosphate dehydrogenase was inhibited with iodoacetate, which reacts with its active site cysteine sulfhydryl group. Which glycolytic intermediate would you expect to accumulate most rapidly, and why?Choose which enzyme is likely deficient based on the symptoms described below: Elevated blood lactate, alanine and pyruvate a) lactate dehydrogenase d) citrate synthase c) pyruvate dehydrogenase d) pyruvate kinase