Why does activation of the phosphorylated b form of glycogen synthase by high concentrations of glucose 6-phosphatemake good biochemical sense?It ensures that glucose is saved when it is abundant and not being used to fuel energy metabolism.It ensures that excess fuel is stored in the most reduced and energy-rich form.It prevents glycogen from being synthesized at the same time as it is being broken down.It prevents the mobilization of glycogen when glucose is already abundant.

The correct answer is b. It ensures that excess fuel is stored in the most reduced and energy-rich…

Answered: Why does activation of the…

Human Anatomy & Physiology (11th Edition)

11th Edition

ISBN:9780134580999

Author:Elaine N. Marieb, Katja N. Hoehn

Publisher:Elaine N. Marieb, Katja N. Hoehn

Chapter1: The Human Body: An Orientation

Section: Chapter Questions

Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...

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Similar questions

in the synthesis of glycogen, the glycogen synthase uses UDP-glucose rather than glucose. Explain in detail way.
Strategies for regulating the central pathways in carbohydrate metabolism vary among different cells in one organism and among organisms. Slight changes in the regulation of enzymes in central metabolism can effectively re-route metabolite traffic through these pathways, just like a small mutation in PFK-1 can convert a healthy cell into a cancerous one. For instance, Gillaspera mold uses an alternative strategy for regulation the TCA and glycolysis. Gillaspera contains a unique isocitrate dehydrogenase that has an allosteric site for citrate. High citrate inhibits isocitrate dehydrogenase in this organism. Gillaspera also lacks a citrate binding site on PFK-1, so this variant of the enzyme is not affected by citrate concentrations at all. Gillaspera lacks the enzymes ethanol dehydrogenase and lactate dehydrogenase and no carbons are lost in its unique fermentation product. Would high glucose in these organisms lead to production of carbon dioxide from glucose catabolism?…
In class, I mentioned that fructose is metabolized differently in the liver compared to glucose. Refer to the figure shown below to calculate the number ofATPs you would expect from the metabolism of fructose in the liver. Show your work! Fructokinase Fructose Fructose-1-P АТР ADP Aldolase B Dihydroxy- acetone phosphate Glyceraldehyde АТР Triose kinase Triose phosphate isomerase ADP 4 - Glyceraldehyde-3-P Glycolysis Руruvate Acetyl-CoA Fatty acids and triglycerides
For each of the following situations, predict the major concequences for glycogen metabolism. Explain your logic in a few sentences. Will the amount of glycogen be higher or lower than the normal or unchanged. a) Effect of mutation Y194F in glycogenenin on glycogen synthesis. b) Effect on the loss of the gene that encodes inhibitor I of protein phosphatase I on both glycogen phosphorylase and glycogen synthase. c) Effect on the substrate analog shown below in glycogen synthesis (hint: what is the normal reaction sequence? At which step in the pathway does this sequence become blocked and why?)
Explain the purpose of the glycerol 3 phosphate shuttle (Don’t worry about the mechanism, just the purpose of the shuttle. Just one sentence here!). Suppose a cell could only rely on the glycerol 3 phosphate shuttle and not the malate-aspartate shuttle, how would that affect the amount of ATP that could be generated from the complete oxidation of 1 molecule of glucose in that cell? How would this change the amount of ATP that could be generated from the complete oxidation of 1 molecule of palmitate in this cell?
Which of the following biochemical reactions should be classified as endergonic (endothermic)? conversion of glucose into amylopectin conversion of lactose into glucose and galactose conversion of glycogen into glucose conversion of sucrose into glucose and fructose conversion of amylose into glucose
Fill in the blanks below (input numbers only!) about the metabolism of hexanoic acid, a fatty acid that is one of the components of vanilla, and whose formula is CH3(CH2)4COOH: First, the fatty acid is activated by attaching CoA, which costs ATP molecules. The fatty acid is then broken down through a beta-oxidation spiral, to make acetyl CoA molecules. This will require "turns" of the beta-oxidation process. Since each turn of the cycle yields ATP molecules, and each acetyl COA will yield ATP molecules by going through the rest of its metabolism, the net ATP molecules produced from one molecule of this fatty acid will be
Which one of the following statements about PEP (phosphoenolpyruvate) synthesis is correct? Pyruvate can be converted to PEP by a combination of reactions that use energy from two different types of nucleotide triphosphate Pyruvate can be converted to PEP by pyruvate kinase via a single reaction. Pyruvate can be converted to PEP by a mutase. Pyruvate is converted to PEP by the citric acid cycle.
Phosphoribosyltransferase (PRT) catalyzes the attachment of a salvaged purine nitrogenous base on the activated form of ribose-5-phosphate called 5-phosphoribosyl- α α-pyrophosphate ( α α-PRPP). True Or False
Which of the following is NOT a regulatory mechanism for catabolism and anabolism? Phosphorylation of enzymes in glycogenesis and glycogenolysis Modulation of enzymes in glycolysis and the aerobic stage of cellular respiration by intermediates and products of the pathway Conversion of pyruvate to alanine Differences in enzymatic activities in response to variations in the concentration of substrates Activation of gluconeogenesis
One of the earliest responses to cellular injury is a rapid increase in the levels of enzymes in the pentose phosphate pathway. About ten days after an injury, levels of glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase in heart tissue are 20 to 30 times higher than normal. However the levels of glycolytic enzymes are only 10% to 20% of normal. Explain this phenomenon.
Otto Warburg made an interesting observation in the 1930s about cancer cells using the fermentation pathway to catabolize pyruvate even when the oxygen supply seemed sufficient for oxidative phosphorylation. One modern explanation for this “Warburg Effect” is that it protects the cancer cells from damage from free radicals. Provide a biochemical rationale for this explanation.

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