10. Phosphofructokinase 2 and.m fructose- 2,6-bisphosphatase have roles in both gluconeogenesis and glycolysis. Which of the following statements are true in regards to this enzyme? A. its activity will not be affected by hormonal signaling OB. it can act as a switch between gluconeogenesis and glycolysis OC. when phosphorylated phosphofructokinase 2 is more active and will make fructose-2,6-bisphosphate OD. an increased insulin to glucagon ratio will lead to the activation of fructose-2,6- bisphosphatase O E. phosphofructokinase 2 is allosterically modified by fructose-1,6-bisphosphate

10. Phosphofructokinase 2 and.m fructose- 2,6-bisphosphatase have roles in both gluconeogenesis and glycolysis. Which of the following statements are true in regards to this enzyme? A. its activity will not be affected by hormonal signaling OB. it can act as a switch between gluconeogenesis and glycolysis OC. when phosphorylated phosphofructokinase 2 is more active and will make fructose-2,6-bisphosphate OD. an increased insulin to glucagon ratio will lead to the activation of fructose-2,6- bisphosphatase O E. phosphofructokinase 2 is allosterically modified by fructose-1,6-bisphosphate

Biochemistry

6th Edition

ISBN:9781305577206

Author:Reginald H. Garrett, Charles M. Grisham

Publisher:Reginald H. Garrett, Charles M. Grisham

Chapter22: Gluconeogenesis, Glycogen Metabolism, And The Pentose Phosphate Pathway

Section: Chapter Questions

Problem 8P

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1.a. Given what you know about glycolysis and gluconeogenesis, does it make sense that insulin activates PDH phosphatase? Why? b.How do vitamins increase to the breadth of chemical reactions available within a biological system?
1. State if true or false a. Gluconeogenesis is the exact opposite of the glycolytic pathway b. The end-product of glycolysis is Acetyl CoA c. There is no enzyme being secreted in the stomach for carbohydrate digestion d.Glycerol 3-phosphate shuttle, which is active in skeletal muscles and in the brain, bypasses Complex I and II of ETC resulting to less energy produced compared to malate-aspartate shuttle. e. Insoluble NSP has high water holding capacity and will increase the intestinal transit time of digesta.
What is the effect of a defective a(1→ 4) phosphatase in Pompe's disease (GSD II)? O Accumulation of abnormal, unbranched glycogen, leading to heart or liver failure and short fife expectancy O Glycogen accumulation in heart, leading to heart failure, muscle weakness, short life expectancy O Absence of UDP-glucose conversion to glycogen, leading to lack of muscle glycogen, exercise intolerance Glycogen accumulation due to lack of glucose-6-phosphate conversion to glucose, leading to liver enlargement, hypoglycemia, short life expectancy O Lack of complete degradation of glycogen to glucose. leading to mild hypoglycemia, enlarged liver and muscle weakness Submit Request Answer
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 ketogenesis
1. Draw a detailed labelled diagram and discuss the hormonal (epinephrine orglucagon) regulation of glycogen phosphorylase. 2. Provide your own diagrammatic representation for the entry of any TWOcarbohydrates: mannose or lactose or sucrose or glycerol into the glycolyticpathway
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
A. What would happen in the Krebs cycle with the loss of activity of phosphoglycerate kinase? What would happen in glycolysis? 10. What happens to glycolysis with the addition of high amounts of citrate? What happens to ETS? 11. What happens in the Krebs cycle with a block in fumerase? 12.If an amino acid enters the Krebs cycle at the acetyl CoA entry point, how much more ATP is being made than if it enters at a keto-glutarate?
2. (a) ( In contrast to the pyruvate dehydrogen- ase complex, the a-ketoglutarate dehydrogenase (aKGDH) complex is not up- or downregulated by phosphorylation or dephosphorylation. However, the complex exhibits cooperativity modulated by the presence of ADP, ATP, inorganic phosphate (Pi), and Ca2+, as illustrated by the diagram on the right for the bovine kidney enzyme complex. Note in the diagram how the addition of 10 μM Ca2+ shifts the affinity of the enzyme complex for aKG from 20 mM Pi/-Ca2+ to 20 mM Pi/+Ca2+. Calcium especially en- hances the cooperative influence of ADP and ATP. Using the expanded copy of the diagram at the end of the problem set, estimate the change in S0.5 (re- member that for allosteric enzymes S0.5 corresponds to KM of a nonallosteric enzyme) for the enzyme complex in the presence of 20 mM Pi/-Ca2+ and in the presence of 20 mM Pi/+Ca2+. Compare similarly the change in S0.5 for the enzyme in the presence of 20 mM Pi/-Ca2+ plus 1.6 mM ADP to the enzyme in the…
a. In the TCA cycle, which of the following combines with acetyl CoA to form a 6-carbon compound? i. oxaloacetate ii. thiamine iii. glucose iv. pyruvate b. The last step in glycolysis is the transfer of phosphoryl group from phosphoenolpyruvate to ADP catalyzed by pyruvate kinase. i. True ii. False
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,
1. Is glycolysis catabolic or anabolic? Discuss the importance of glycolysis. 2. What triggers gluconeogenesis? Then, what is the main purpose of gluconeogenesis?
7) What are the major pathways of glucose utilizations that are vary with physiological conditions, and organisms? (Describe the three possible fates of pyruvate) .