Why is it physiologically advantageous for the pancreas to use GLUT2, with a high Kyglucose entry into ß cells?M, as the transporter that allowsGLUT2 is a low-affinity glucose transporter; therefore, insulin is only released in response to elevated circulatingglucose levels.GLUT2 is a low-affinity glucose transporter; therefore, glucagon is only released in response to elevated circulatingglucose levels.GLUT2 is a high-affinity glucose transporter; therefore, glucagon is released continuously in response to the constantrate of glucose uptake.GLUT2 is a high-affinity glucose transporter; therefore, insulin is released continuously in response to the constant rateof glucose uptake.

Two hormones regulate glucose hemostasis in the blood: insulin- released in response to high blood…

Answered: Why is it physiologically advantageous…

Biochemistry

6th Edition

ISBN:9781305577206

Author:Reginald H. Garrett, Charles M. Grisham

Publisher:Reginald H. Garrett, Charles M. Grisham

Chapter27: Metabolic Integration And Organ Specialization

Section: Chapter Questions

Problem 14P

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The epinephrine-mediated “amplificationcascade” of Figure 24.14 has six steps, all of which are catalyticwith one exception. This cascade leads to the activation of glycogenphosphorylase. This enzyme acts in turn on glycogen to yieldglucose-1-phosphate (G-1-P).(a) Which step is not catalytic?(b) If each catalytic step had a turnover (molecules of substrateacted on per molecule of enzyme) of 10, how many moleculesof G-1-P would result from one molecule of epinephrine?(c) What is the biochemical advantage of such a cascade?(d) How is the amplification cascade of this questionreversed?
Mutations in glucokinase which lower the kcat for the enzyme or elevate the Km for glucose result in mild to moderate elevation of blood glucose. Explain how these mutations cause diabetes-like symptoms in patients.
Compare the localization of GLUT4 with that of GLUT2 and GLUT3, and explain why these localizations are important in the response of muscle,adipose tissue, brain, and liver to insulin
Researchers investigating the role of fat metabolism in diabetes generated PPAR peroxisome proliferator-activated receptor gamma (PPARγ) knockout mice. When fed a high fat diet, these mice did not gain extra adipose tissue or display significant weight gain. Explain why this is the case.
The antidiabetes drugs known as thiazolidinediones induce the production of glycerol kinase in adipocytes. Explain why this would decrease the concentration of serum fatty acids, which are often elevated in diabetics.
Many diabetics do not respond to insulin because of a deficiency of insulin receptors on their cells. How does this aff ect (a) the levels of circulating glucose immediately after a meal and (b) the rate of glycogen synthesis in muscle?
Diabetes often results in the production of reduced levels of insulin. Researchers claim that a drug that binds to and blocks the active site of GSK3 might mimic the role of insulin in the pathway shown in Figure 2. Provide reasoning to justify the researchers' claim.
Stimulation of a certain Gs protein–coupled receptor activates protein kinase A (PKA). Predict the eff ect of PKA activation on the following substrates of PKA: (a) acetyl-CoA carboxylase, (b) glycogen synthase, (c) hormone-sensitive lipase, and (d) phosphorylase kinase.
Which TCA component is syphoned off to increase glucose production via gluconeogenesis when glucose consumed levels are low?
HbA1c is used to monitor blood glucose levels because hemoglobin is the only protein in blood that is covalently modified by glucose. True False Insulin Glargine is a long-acting form of insulin that is synthesized with several D-amino acids that slow its proteolytic degradation and extend the half-life of the insulin Glargine molecule. True False
Glycogen synthase in the liver is a target for phosphorylation by two protein kinases. What are these two protein kinases and how are they independently regulated by glucagon and insulin to regulate glycogen biosynthesis?
Does the allosteric regulation induced by insulin activate (or repress) phosphofructokinase-1 activity?

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