How many FADH2 _____& ATP _____are produced from the beta oxidation of Lauric Acid?
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Q: How many moles of ATP are produced from the beta oxidation of Lauric Acid? o 60 ATP o 50 ATP o 70…
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Q: How many NADH _____& ATP _____are produced from the beta oxidation of Lauric Acid?
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How many FADH2 _____& ATP _____are produced from the beta oxidation of Lauric Acid?
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- The interconverison of DHAP and GAP greatly favors the formation of DHAP at equilibirum. Yet the conversion of DHAP by triose phosphate isomerase proceeds readily. Why?A strain of mice has been developed that lack the enzyme phosphorylase kinase. Yet, after strenuous exercise, the glycogen stores of a mouse of this strain are depleted. Explain how this depletion is possible.TPI deficiency is a rare human condition. Patients who lack TPI cannot convert the triose dihydroxyacetone phosphate into glyceraldehyde 3-phosphate.What happens to glycolysis in TPI patients?TPI patients suffer from chronic hemolytic anemia (abnormal breakdown of red blood cells) and have variable neuromuscular dysfunctions, including muscle weakness, poor muscle tone, and atrophy. Most die of respiratory failure during childhood. Explain why TPI-deficient patients exhibit these conditions using the diagram to justify your answer. TPI is enzyme 5.G6PD deficiency is one of the most common human genetic conditions, affecting about 40 million people worldwide. Patients suffer from hemolytic anemia when exposed to certain drugs, viral or bacterial disease, or fava beans.
- Why does the lack of glucose 6- phosphatase activity in the brain and muscle make good physiological sense?It is absolutely not necessary to produce amylase in an active form in our body. But it is not in the case of trypsin. Given reasons.Phosphoglucokinase catalyzes the phosphorylation of the C6-OH group of G1P. Why is this enzyme important for the normal function of phosphoglucomutase?
- What are the metabolic effects of not being able to produce the M subunit of phosphofructokinase?In angiogenic endothelial cells, pyruvate is converted to lactate (generating 2 ATP per glucose) rather than being completely oxidized (which would generate ~32 ATP by oxidative phosphorylation). Explain why angiogenic cells generate ATP anaerobically.During hyp[erglycemia or diabetes - what two regulatory enzymes are active? Why are they active?
- In McArdle's disease, a type of glycogen storage disease, there is a total deficiency of muscle glycogen phosphorylase. An individual with such disease is not able to exercise strenuously and experiences muscle cramps. Exercise leads to higher than normal levels of cellular ADP and Pi. Besides, lactic acid does not accumulate, as in the case of a normal individual. Explain the chemical imbalances shown in McArdle's discase.Von Gierke’s disease is also known as glycogen storage disease type I. Patients with von Gierke’s disease lackglucose 6-phosphatase activity. Two prominent symptoms of this disorder are fasting hypoglycemia and lactic acidosis (elevated lactate levels in the blood), especially during strenuous exercise. Explain why these symptoms occur. What chemical reaction does this enzyme catalyze? Which pathways involve this enzyme? Lacking thisthe enzyme will cause impairment of which pathways?• Pls consider what pathways are affected by Von Gierke’s disease. Include in your explanation involving Cori’s cycle. can you please do not write by your hand? I mean computer if you can. thank youVon Gierke’s disease is also known as glycogen storage disease type I. Patients with von Gierke’s disease lackglucose 6-phosphatase activity. Two prominent symptoms of this disorder are fasting hypoglycemia and lactic acidosis (elevated lactate levels in the blood), especially during strenuous exercise. Explain why these symptoms occur. What chemical reaction does this enzyme catalyze? Which pathways involve this enzyme? Lacking thisenzyme will cause impairment of which pathways?• Pls consider what pathways are affected by Von Gierke’s disease. Include in your explanation involving the Cori’s cycle.