Question

(briefly explain and answer questions 1-4)

1.During fasting, muscle protein breakdown and lipolysis in adipose tissue are accelerated. How do these changes enhance glucose production by gluconeogenesis in liver?

2.Why might a genetic mutation in glucose 6-phosphate dehydrogenase alter the rates of synthesis of lipids?

3.How many ATP molecules would you expect from the conversion of a-ketoglutarate to malate in tightly coupled mitochondria?

4.The rate of oxidation of pyruvate by tightly coupled mitochondria is decreased if palmitoyl carnitine is added. Discuss the mechanism for this change.

Answer 1

1) as glucose is the mean in primary source of energy in the body which goes through glycolysis and electron transport chain pathway to generate ATP . there is a homeostasis system in the human body by the use of different endocrine organs and metabolic systems to regulate the blood glucose level. During fasting there is a decrease in the blood glucose level which is called as hypoglycemia. Hypoglycemia stimulates pancreatic Alpha cells to release glucagon and inhibits the release of of insulin by beta cells. this glucagon released in the blood reaches to the liver and stimulate the hepatocytes by the g coupled receptors which lead to the release of secondary messengers known as cyclic adenosine monophosphate which further leads to the activation of the enzyme by the phosphorylation. This activation of the enzymes leads to the increased gluconeogenesis in the hepatocytes. Gluconeogenesis is the process of forming glucose by the body from non carbohydrate source like protein fat lactic acid .etc so this increase in the gluconeogenesis is mainly mediated by the the hyperglycemic hormone named glucagon.

2) as we all know that the main enzyme for generating the NADPH reducing potential is glucose 6 phosphate dehydrogenase which is the main enzyme of hexose monophosphate pathway. Glucose 6 phosphate enzyme generate NADPH which is helpful in many detoxification processes RBC membrane stabilization cholesterol and fatty acid synthesis detoxifying the oxygen radicals and many more. NADPH excess a mediator in the synthesis of of fatty acids and cholesterol if there is a mutation in the glucose 6 phosphate synthesis which leads to the increase in the enzyme activity e for decrease in the enzyme activity which leads to the the increase synthesis of NADPH or decrease synthesis of NADPH. Which leads to the the defective metabolism of fatty acid and cholesterol which further leads to the obesity if enzyme activity increased or weight loss if enzyme activity is decreased.

3) first of all before knowing about the Alpha ketoglutaric acid we need to get some knowledge about the glucose metabolism. Glucose metabolism is mainly done by these pathways the first one is glycolysis the second one is pyruvate dehydrogenase and the third one is crab cycle and finally the redox potential generated will be converted to ATP by the electron transport chain. Alpha ketoglutaric acid is the the metabolic product in the krebs cycle of glucose metabolism. in krebs cycle the Alpha ketoglutaric acid converted to succynyl coA which leads to the generation of 1 NADH2 and co2. Nashik senile coenzyme a converted to succinate which leads to the generation of of 1 GTP. Now succinate converted to ew fumarate which leads to the generation of 1 FADH2. Finally the fumarate converted to melate.in this pathway from Alpha ketoglutaric acid to malate there is total generation of 1 GTP +1NADH2 +1FADH2 = 1ATP+3ATP+ 2ATP= 6ATP.

4) as we all know that the palmitoyl Carnitine is a fatty acid. In the metabolism of the fatty acids the fatty acids are converted into acetyl coenzyme a by the process of beta oxidation. So acetyl coenzyme a is the product generated due to the the metabolism of pyruvate by pyruvate dehydrogenase. So if on adding the palmitoyl Carnitine the amount of acetyl coenzyme a increases which leads to the competitive inhibition of pyruvate dehydrogenase so on inhibition of pyruvate dehydrogenase the metabolism of pyruvate is also decreased.