Chapter 15: Problem 2
6-Phosphofructo-1-kinase activity can be decreased by all of the following except A. ATP at high concentrations. B. cirrate. \(\mathrm{C}_{1} \mathrm{AMP}\) D. low pH. E. decreased concentration of fructose 2,6 -bisphosphate.
Chapter 15: Problem 2
6-Phosphofructo-1-kinase activity can be decreased by all of the following except A. ATP at high concentrations. B. cirrate. \(\mathrm{C}_{1} \mathrm{AMP}\) D. low pH. E. decreased concentration of fructose 2,6 -bisphosphate.
All the tools & learning materials you need for study success - in one app.
Get started for freeAlcohol intoxication can lead to hypoglycemia especially if the alcohol is consumed by an undernourished individual or after strenuous exercise. In both cases the hypoglycemia results from the inhibitory effects of alcohol on hepatic gluconcogenesis and occurs under circumstances of heparic glycogen depletion. Alcohol potentiates the hypoglycemic effect of insulin so diaberics who have self-administered insulin and then consumed alcohol are at increased risk. Insulin promotes hypoglycemia by a varicty of mechanisms including all of the following crcept A. inactivating a transcription factor for genes of key gluconeogenic enzymes. B. inhibiting lipolysis in adipose tissue, thus decreasing the energy supply for gluconcogenesis in the liver. C. decreasing levels of \(\mathrm{CAMP}\). D. increasing activation of phosphoprotein phosphatase. E. increasing the activity of \(c A M P\) -response element binding protein (CREB) and its binding to the cAMP-response element (CRE).
Patients with hereditary fructose intolerance are deficient in the liver form of the enzyme aldolase. Consumption of fructose leads to a depletion of ATP and \(P\), in the liver, which, in turn, leads to cell damage, Much of the cell damage can be attributed to the inability to maintain normal ion gradients by ATP-dependent pumps. The products initially produced by aldolase action on the substrate formed from fructose are A. two molecules of dihydroxyacetone phosphate. B. rwo molecules of glyceraldchyde 3 -phosphate. C. rwo molecules of lactate. D. dihydroxyacetone phosphate and glyceraldehyde 3 -phosphate. E. dihydroxyacctone phosphate and glyceraldehyde.
Glucose 6 -phosphatase, which is deficient in Von Gierke disease, is necessary for the production of blood glucose from A. liver glycogen. B. fructose. C. amino acid carbon chains. D. lactose. E. all of the above.
Glucokinase A. has a Sos greater than the normal blood glucose concentration. B. is found in muscle. C. is inhibited by glucose 6 -phosphate. D. is also known as the GLUT-2 protcin. E has glucose 6 -phosphatase activity as well as kinase activity.
Malignant hyperthermia is a genetic abnormality in which exposure to certain agents, especially the widely used general anes. thetic halothane, produces a dramatic rise in body temperature, acidosis, hyperkalemia, and muscle rigidity. Death is rapid if the condition is untreated and may occur the first cime a susceptible person is anacstictiad. The defect causes an inappropriate release of \(\mathrm{Ca}^{2+}\) from the sarcoplasmic reticulum of muscle. Many heat-producing processes are stimulated in an uncontrolled fashion by the release of \(\mathrm{Ca}^{2+}\), including glycolysis and glycogenolysis. Thosphorylation-dephosphorylation and allosteric accivation of enzymes play roles in stimularing glycogen degradation. All of the following result in enzyme activation except A. phosphorylation of phosphorylase kinase. B. binding of AMP to phosphorylase b. C. phosphorylation of phosphorylase. D. phosphorylation of protein kinase \(A\). E. dephosphorylation of glycogen synchase.
What do you think about this solution?
We value your feedback to improve our textbook solutions.