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- Indicate what will happen ( increase, decrease or no effect) tothe activity of the enzyme or rate of the metabolic pathway in the given conditions a. release of glucagon in the blood to the activity of carnitine acyl transferase 1 b. high malonyl CoA to the activity of carnitine acyl transferase I C. Epinephrine to the activity og glycogen synthase d. high citrate to the activity of acetyl CoA carboxylase e. high acetyl CoA to ketogenesisExplain why inhibiting the activity of acetyl-CoA carboxylase might not affect a person’s body mass.26. Which of the following statements is correct? A. Insulin can activate pyruvate carboxylase B. More energy in the form of ATP is required to synthesize glucose from pyruvate than can be obtained from glucose by glycolysis alone C. Fructose-2,6-bisphosphate is a modulator that can stimulate either glycolysis or gluconeogenesis, depending on cellular glucose concentration D. All of the above
- T/F High intracellular concentrations of AMP would increase the ATP-synthesis pathways 2 A mutation that does not allow for the phosphorylation of acyl CoA carboxylase would result in: A Unregulated ß-oxidation of fatty acids B. Build-up of malonyl-CoA C. Influx of fatty acids into the mitochondria D. Inhibition of acetyl-CoA synthetasesCompare and contrast the following items related to lipid metabolism. Cite their main similarities/or differences. 1. Steroid hormones vs. prostaglandins (in terms of their biosynthetic pathways). 2. Fatty acid synthase complex vs. pyruvate dehydrogenase complex.A deficiency in sorbitol dehydrogenase cause all of the following except: Select one: O a. pathologic alternations related to Diabetes mellitus b. no lactose synthesis O c. lack of sperm motility O d. no fructose synthesis
- vny can acetone sometimes be detected in the breath of patients with type 1 diabetes? A. Glucagon signaling is faulty, leading to an excess of oxaloacetate, which enables acetyl-CoA to enter the citric acid cycle, therefore resulting in the production of ketone bodies including acetone OB. Insulin signaling is faulty, so excess malonyl-CoA is generated, which leads to excess acetyl-CoA from beta oxidation Oc. None of the other answers is correct OD. Insulin signaling is correct, but excess acetyl-CoA is generated anyway, leading to the production of ketone bodies including acetone O E. Insulin signaling is faulty, fatty acids are catabolized to acetyl- COA despite high blood glucose, and excess acetyl-CoA is converted to ketone bodies,7. During several days, Patient A got a meal with high caloric value, and Patient B- with a low caloric value. What are the differences in the lipid metabolism in these two patients? What is the insulin/glucagon ratio in these patients after a meal? Which metabolic pathways rather activated in Patient A and how is it being controlled? 8. The adipose tissuc is not only store triacylglycerols but also is active endocrine organ. Explain this function of the adipose tissuc. For that: a) explain the sclinical obesity and possible conscouences of the discase: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?
- Compare and contrast the following items related to lipid metabolism. Cite their main similarities/or differences. 1.lysophosphatidylcholine vs. phosphatidylethanolamine 2.trimyristin vs. triolein. 3. ACP vs. carnitine-acyl transferase.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.In the context of fatty acid oxidation to acetyl CoA, indicate whether each of the following substances is involved in (1) fatty acid activation, (2) fatty acid trans-port, or (3) b-oxidation pathway. More than one choice may be correct in a given situation. a. AMp b. FAD c. Acyl CoA d. H2O