A patient has a defective liver FBPase-2 enzyme, the enzyme that converts F2,6P into F6P. Thisenzyme is inactive. What effect would this have on the differential regulation of glycolysis andgluconeogenesis in liver cells? How would this affect a person's ability to respond appropriately to alow blood sugar state? What about a high blood sugar state?

Fructose 2,6-BIsphosphate is a potent regulator of glycolysis and gluconeogenesis. It has a special…

Answered: A patient has a defective liver…

Biochemistry

9th Edition

ISBN:9781319114671

Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Publisher:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Chapter1: Biochemistry: An Evolving Science

Section: Chapter Questions

Problem 1P

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Similar questions

Pancreatic β cells express a receptor for fatty acids. Fatty acid binding to the protein appears to stimulate insulin secretion. Does this phenomenon make metabolic sense?
In the indicated tissues, how will each process or the activity of each enzyme below be affected by the signal sent upon Glucagon secretion? Use an up (t) or down (1) arrow or NC (no change). (Hint: Decide what pathways will be up-regulated first, then look at the enzymes below!) + Triacylglygerol Lipase (Adipocytes) Phosphofructokinase-2 (Liver) Insulin secretion (Pancreas) Pyruvate Kinase (Muscle) Glycogen Phosphorylase (Liver) Phosphofructokinase-1 (Liver) Fructose-1,6-bisphosphatase 1 (Liver) Fatty Acid Biosynthesis (Liver) PEP Carboxxkinase (Liver) Phosphorylation of Perilipins (Adipocytes) Adenylate Cyclase (Liver) Glycogen Synthase (Liver) Acetyl CoA Carboxylase Hexokinase II (Muscle)
What is caused (indirectly) by the binding of a glucagon molecule to its receptor on the surface of a liver cell? Phosphorylation of glycogen phosphatase, which results in it becoming less active. Dephosphorylation of glycogen synthase, which results in it becoming less active Phosphorylation of glycogen phosphorylase, which results in it becoming more active Dephosphorylation of phosphorylase kinase, which results in it becoming more active. Phosphorylation of glycogen synthase, which results in it becoming more active
Lipodystrophy is a condition in which an individual lacks adipose tissue. The muscles and liver from such individuals are insulin resistant, and both tissues accumulate large amounts of triacylglycer ols (hyperlipidemia). The administration of leptin partly ameliorates this condition. What does it indicate about the relation of adipose tissue to insulin action?
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?
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.
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?
Why would LDH be up- or down-regulated depending on location of cancer cells? Anaerobic cancer cells enhance rates of ATP production and rely on pyruvate to lactate conversion. LDH5 expressed can vary in favoring pyruvate for conversion to lactate (anaerobic metabolism). Aerobic compartments in newly formed fibrobasts and vessels use lactate to convert to pyruvate for oxidative phosphorylation and favor lactate conversion to pyruvate by LDH1 (aerobic metabolism). Lactate dehydrogenase is upregulated in both cancer cells and supporting stroma and vessels, thus only LDH5 is upregulated showing enhanced expression levels and thus presence at the plasma membrane to increase levels of lactate for export, LDH1 levels are always consistent. LDH1 is upregulated in response to the export of lactate by MCT1, while LDH5 is down-regulated Neither LDH1 or LDH5 are both consistently expressed, regardless of oxygen levels
What is the effect of insulin on the committed step of glycolysis in the liver? Describe the mechanism by which insulin can affect the activity of this enzyme in the liver?
Which of the following are mechanisms that prevent the liver from using up glucose that is more urgently required by other tissues? (select all that apply) Group of answer choices Glucokinase (the liver's version of hexokinase) has a lower affinity for glucose than hexokinase does GLUT2 has a lower affinity for glucose than GLUT4 does The liver produces insulin when blood glucose levels are low The liver does not express a phosphofructokinase enzyme The liver increases glycolysis in response to glucagon
For an individual whose liver is regulated by glucagon binding, when energy is needed - what is the major source of carbon skeletons used to produce TCA cycle intermediates? Amino acids Glucose Fatty acids Glyoxylate
In type I diabetes mellitus, excessive production of acetyl-CoA may surpass the body’s capacity to oxidize it. As a result, acetoacetate, β-hydroxybutyrate, and acetone (ketone bodies) accumulate. When generated in large amounts, blood pH falls, thereby reducing the capacity of red blood cells to carry oxygen. Explain in general terms how high concentrations of ketone bodies may result in a fatal coma.

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