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Investigate short-chain (12 carbons or less) fatty acid metabolism: Monitor ketone body formation in the blood...

Investigate short-chain (12 carbons or less) fatty acid metabolism: Monitor ketone body formation in the blood Results: Interestingly, when Jessie was fed a solution containing short-chain fatty acids and again fasted, plasma acetoacetate and γ-hydroxybutyrate concentrations increased.

15. What does this result tell you about Jessie? A. Nothing B. Something, but not clear what C. One of the enzymes of the β-oxidation pathway must be deficient D. There must be a problem with specifically long-chain fatty acid transport, not with β-oxidation E. There must be a problem with lipolysis of TAGs to produce FAs

16. If Jessie has a problem transporting fatty acids into the mitochondria for β-oxidation, then there may be another consequence that we have not yet uncovered! Consider this question: what do you think would happen to fatty acids that arrive at the liver for β-oxidation but then cannot be metabolized because they cannot enter the mitochondria? (Hint: They are not transported back to adipose tissue or excreted in the urine!) A. They are stored as TAGs in the liver B. They are used by the liver to make glucose C. They are used by the liver to make ketone bodies

17. In a previous investigation you also found evidence that the specific problem is likely to be the inability to transport long-chain fatty acids into the mitochondria, since short-chain acids are processed normally. The exact problem and cause still remain to be determined, so you must continue with your investigations. Consider this question before returning to additional investigations: Which of the following proteins are involved in the transport of long-chain fatty acids into the mitochondria? (Select ALL that apply!) A. Pyruvate dehydrogenase B. Carnitine acyltransferase I (CAT I) C. Citrate synthase D. Carnitine acyltransferase II (CAT II) E. Aldolase F. Acyl-CoA dehydrogenase

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15. What does this result tell you about Jessie?

Answer:-

When human body is starved or not fed carbohydrates and given fatty acids or short chain fatty acids, liver swithches from carbohydrate utilization and fatty acid synthesis mode to fatty acid oxidation and ketone body production. By Producing these ketone bodies it supplies each to mind, heart, muscle tissue and kidneys.

Acetoacetate and 3-hydroxy butyrate with CH3)2CO are primary ketone bodies created. Acetoacetate (AcAc) and beta hydroxy butyrate (3BH) are short chain - 4carbon natural acids that can uninhibitedly diffuse crosswise over cell layers.

Under typical oxygen consuming conditions glucose and unsaturated fats are utilized to acetyle CoA by glycolysis and beta oxidation. Be that as it may, amid fasting the intracellular glucose levels turn out to be too low which clears route for gluconeogenesis, where acetyle coA is occupied to frame ketone bodies(ketogenesis).ketone bodies assume a decent job in decreasing glucose use and lessening proteolysis. These are the primary elective vitality saves for mind cells when glucose levels are low amid fasting. Acetyle coA carboxylase production is reduced and it favours lypolysis in adipocytes favouring ketogenesis. Another enzyme HMG coA produced by liver in starvation state to favour ketogenesis. Fatty acid biosynthesis is ceased and lipolysis takes place to favour ketone body production for energy supply to all organs during fasting or starvation.

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