Phosphoenolpyruvate carboxykinase (PEPCK, figure below)catalyzes first committed (rate-limiting) step in hepatic gluconeogenesis, namely the reversible decarboxylation of oxaloacetate to phosphoenolpyruvate (PEP) and carbon dioxide. This reaction can occur using either ATP or GTP as a source of the phosphate.Which following mutation can potentially improve the binding affinity of the substrate for this enzyme? a. LYS254ARG b. LYS254ASP c. ARG333GLU d. THR255GLY
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Phosphoenolpyruvate carboxykinase (PEPCK, figure below)catalyzes first committed (rate-limiting) step in hepatic gluconeogenesis, namely the reversible decarboxylation of oxaloacetate to phosphoenolpyruvate (PEP) and carbon dioxide. This reaction can occur using either ATP or GTP as a source of the phosphate.Which following mutation can potentially improve the binding affinity of the substrate for this enzyme?
a. LYS254ARG
b. LYS254ASP
c. ARG333GLU
d. THR255GLY
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- For each of the following conditions, state whether this condition would be occurring during gluconeogenesis, glycolysis, or both in liver cells. a. Transporting malate from the cytosol into the mitochondria. _____________ b. Transporting pyruvate from the cytosol into the mitochondria. _____________ c. We would have an increased (or increasing) concentration of F26BP. __________ d. Increased concentration of F6P.__________ e. Hexokinase IV (or glucokinase) is found in the nucleus of the cell. __________ f. The enzyme that synthesizes/breaks down F26BP is phosphorylated. __________ g. Elevated levels of glucagon in the blood. ____________If all of the pentose phosphate pathway is functioning (both oxidative and non-oxidative portions), 6 glucose 6-phosphates are used, how many glucose 6-phosphates can be regenerated for use in the liver?In the intestine, the triacylglycerols must be converted to fatty acids and glycerol by hydrolytic enzymes before transport into enterocytes. Afterward, fatty acids and glycerol are reconverted into triacylglycerols and then packaged into chylomicrons. Suggest why this energy-requiring process is used instead of a direct transport of triacylglycerols into enterocytes.
- If glucagon binds to the liver cell, what is the expected regulation of the bifunctional enzyme phosphofructokinase-2/fructose-2,6-bisphosphatase and how would the levels of fructose-2,6-bisphosphate be impacted?True or false 1. Cytochrome p450 is considered to be the “universal oxygenase” 2. In alzheimer’s and Parkinson’s diseases, there is hyperphosphorylation of tau that leads to the intracellular accumulation of tau in the form of neurofibrillary tangles.Concerning the reciprocal regulation of phosphofructokinase and fructose-1,6-bisphosphatase in the liver, which of the following statements are true? Select all that apply A.The default activity of the cell favors activity of phosphofructokinase-2 being activated, generating fructose-2,6-bisphosphate that serves as a potent allosteric activator of phosphofructokinase B.Glucagon binding ensures that the levels of fructose-2,6-bisphosphate drop within the liver cell C.In the presence of ATP and fructose-2,6-bisphosphate, phosphofructokinase will be fully inhibited and glycolysis turned off D.High levels of fructose-2,6-bisphosphate signals for activation of gluconeogenesis and inhibition of glycolysis E.Glucagon binding to the liver cell activates a phosphorylation cascade that inhibits activity of phosphofructokinase-2 and activates fructose-2,6-bisphosphatase F.Glucagon binding activates glycolysis as it signals high blood sugar levels
- Leigh syndrome is characterized by psychomotor regression: that is, the progressive loss of mental andmovement abilities. Patients also suffer from lacticacidosis, a condition in which mitochondrial respiration is deficient, so their tissues metabolize glucoseanaerobically, leading to the buildup of lactate. Somepatients with Leigh syndrome have a mutation in themitochondrial gene MT-CO3, which encodes a subunit of the electron transport complex cytochromec oxidase. Other patients diagnosed with Leigh syndrome have a loss-of-function mutation in the nucleargene SURF1, which encodes a factor needed for theassembly of this same enzyme complex.a. How can the same symptoms result from mutationsin a mitochondrial gene and from mutations in anuclear gene?Interestingly, we can measure metabolism through respiration, with what’s called the respiratory quotient. What is it? What does a decrease in the non-protein respiratory quotient (npQR ) tell us about the severity of liver disease? Is the liver in this case relying more on Glycogen or Fat?The disease beriberi, which results from a dietary deficiency of vitamin B1 (thiamine), is characterized by neurologic and cardiac symptoms, as well as increased levels of pyruvate and α-ketoglutarate in the blood. How does a deficiency of thiamine account for the increased levels of pyruvate and α-ketoglutarate?
- Describe one mechanism that leads to continued gluconeogenesis in the liver of T1DM patients, despite already high levels of glucose in the bloodstream.E1 and E2 of the pyruvate dehydrogenase complex is coupled via: (d) Transfer of an acetyl group from TPP to lipoamide a and c b and d (a) Reductive decarboxylation of pyruvate coupled to oxidation of acetylation of lipoamide (c) Transfer of an acetyl group from lipoamide to TPP (b) Oxidative decarboxylation of pyruvate coupled to reduction of acetylation of lipoamideHomocystinuria is caused by a defect in cystathionine beta-synthase (or 13-synthase), which leads to an accumulation of homocysteine in the blood. This accumulation causes symptoms such as a tall, thin frame, flushed cheeks, and osteoporosis (thinning of the bones). These individuals should limit their intake of proteins that contain methionine, such as egg whites. Using your understanding of biochemistry, explain why people with Homocystinuria should not consume egg whites and other such proteins.