5. During prolonged fasting, amino acids derived from muscle proteins andconnective tissue become the main substrate for gluconcogenesis. How doesglutamate enter the gluconeogenesis? For answer:a) write a reaction of the glutamate conversion into a-ketoglutarate, name theenzyme, indicate the encrgy effect of the reaction;b) draw a diagram for the a-ketoglutarate conversion to oxaloacetate andconsequent including of OAA to gluconcogenesis, specify the reactionsassociated with ATP consumption;c) name the hormones that accelerate gluconeogenesis during fasting andregulatory enzymes of the process; and describe the mechanism of signaltransduction by these hormones.

Answered: Image /qna-images/answer/aa317887-21e9-41a0-9f54-6ecdc2f72ab3.jpg

Answered: 5. During prolonged fasting, amino…

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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1) under intracellular conditions, answer : If G3P-DH is inhibited by Iodoacetic acid, which glycolytic intermediate will accumulate most rapidly and why ? 2) How will increased oxaloacetate level in mitochondria affect fatty acid biosynthesis ?
Muscles may become hypoxic during the early stages of exercise, causing lactate to build up. a) Describe in detail how a lack of oxygen might cause lactate to build up in the muscles. b) Explain how lactate (typically thought of as a waste product) may be converted to glucose via gluconeogenesis.
During the initial phase of exercise, muscles can become hypoxic which leads to the buildup of lactate. a) Fully explain how oxygen shortage can lead to the accumulation of lactate in the muscles. b) Describe how lactate (often seen as a waste product) can produce glucose via gluconeogenesis.
6. In an experiment, students used liver tissuc samples to study the cthanol metabolism and the possibility of ethanol conversion into glucose. The ethanol introduction in the investigated medium didn't lead to glucose level increase. Why is it impossible to convert ethanol to glucose? For the answer: a) provide a scheme of gluconcogenesis, indicate the substrates of this process; b) write the reaction of ethanol oxidation in the liver; c) explain whether it is possible to use the metabolites of ethanol catabolism for the glucose synthesis.
Compare the regulation of phosphofuctokinase-1 (PFK- 1) activity and fructose 1,6- bisphosphatase in glycolysis. c) In the B-oxidation of a saturated, even chain fatty acid, four basic steps are involved. Describe these reactions using the degradation of palmitic acid as an example. d) e) Compare the steps involved in the formation of ketone bodies.
Name the molecules used for gluconeogenesis. What are the sources of these molecules? Under what conditions would gluconeogenesis occur?
Q) Glycolysis and Gluconeogenesis are regulated through differential regulation a) What does differential regulation mean? b) Provide an example of a differential regulator from glycolysis (vs gluconeogenesis) • State what enzyme it regulates in glycolysis and what kind of regulator it is • In less than 10 words state what physiological conditions it signals.
(a) What amino acid, other than alanine, can be converted by transaminationto a gluconeogenic precursor? (b) Calculate the cost, in ATP equivalents, of converting two molecules of this amino acid to one molecule of glucose.
During the fed state, which of the following occur(s)? a) insulin stimulation of malonyl CoA formation b) allosteric inhibition of carnitine acyltransferase I c) both a and b d) neither a nor b
Consider oleic acid (18:1∆9): 1. How many NADH will be produced from complete oxidation of this fatty acid? 2. How many FADH2 will be produced from complete oxidation of this fatty acid? 3. Total number of ATP produced from NADH in complete oxidation of oleic acid (exclude transport cost of the fatty acid)? 4. Total number of ATP produced from FADH2 in complete oxidation of oleic acid (exclude transport costs of the fatty acid)? Please provide how you got them.
Phosphoglycerate mutase (PGM) catalyzes the interconversion of 3-phosphoglycerate (3PG) and 2-phosphoglycerate (2PG) in the glycolytic and gluconeogenic pathways. a) To what enzyme class does PGM belong? b) There are two distinct classes of PGM, one which is dependent on 2,3-bisphosphoglycerate (2,3-BPG), dPGM, and one which is not, iPGM. dPGM uses acid base chemistry and a phosphorylated histidine residue to interconvert 3PG and 2PG. The dPGM reaction proceeds with formation of 2,3-BPG as an intermediate. Propose a mechanism for the dPGM-catalyzed conversion of 3PG to 2PG that is consistent with this information. c) What is the purpose of 2,3-BPG (i.e., why does dPGM require it)?
1. Glycolysis & Gluconeogenesisa) a)Write the overall net reaction for glycolysis. b) Write the overall netreaction for gluconeogenesis. c) What is the energy cost (assume ATP≡GTP) of transforming glucose to twopyruvate and back to glucose? d) What enzymes of glycolysis are bypassed in gluconeogenesis? e) What enzymes are unique to gluconeogenesis? f) What enzymes are the sites of regulation in gluconeogenesis? g) Describe how glycolysis & gluconeogenesis are reciprocally regulated.

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