Biochemistry: The Molecular Basis of Life
6th Edition
ISBN: 9780190209896
Author: Trudy McKee, James R. McKee
Publisher: Oxford University Press
expand_more
expand_more
format_list_bulleted
Concept explainers
Question
Chapter 9, Problem 38SA
Summary Introduction
To review:
The way through which high levels of cytoplasmic NADH (nicotinamide adenine dinucleotide reduced) provide a source of NADPH (nicotinamide adenine dinucleotide phosphate) for the synthesis of fatty acid.
Introduction:
Expert Solution & Answer
Want to see the full answer?
Check out a sample textbook solutionStudents have asked these similar questions
One consequence of ethanol addiction is fatty liver disease, an illness in which liver cells accumulate large amounts of triacylglycerols, the esters derived from glycerol and fatty acids. Ethanol is oxidized in the cytoplasm of liver cells by alcohol dehydrogenase and aldehyde dehydrogenase to yield acetate and 2 NADH. Acetate is then transported into the mitochondrion, where it is converted to acetyl-CoA and metabolized in the citric acid cycle. When alcohol is consumed in excessive quantities, the resulting high levels of NADH cause metabolic abnormalities, one of which is high levels of fatty acid synthesis. Fatty acid synthesis, also a cytoplasmic process, uses acetyl-CoA as a substrate and NADPH as a reducing agent. Speculate about how a high level of cytoplasmic NADH provides a source of NADPH for fatty acid synthesis.
One of the consequences of ethanol addiction is fattyliver disease, an illness in which liver cells accumulatetriacylglycerols, the esters derived from glycerol and fattyacids. Ethanol is oxidized in the cytoplasm of liver cells byalcohol dehydrogenase and aldehyde dehydrogenase to yieldacetate and 2 NADH. Acetate is then transported into themitochondrion, where it is converted to acetyl-CoA andmetabolized by the citric acid cycle. When alcohol is consumed in excessive quantities, the resulting high levels ofNADH cause metabolic abnormalities, one of which is highlevels of fatty acid synthesis. Fatty acid synthesis, also acytoplasmic process, uses acetyl-CoA as a substrate andNADPH as a reducing agent. Determine how a high level ofcytoplasmic NADH provides a source of NADPH for fattyacid synthesis.
When the acetyl-CoA produced during β-oxidation in the liver exceeds the capacity of the citric acid cycle, the excess acetyl-CoA forms ketone bodies—acetone, acetoacetate, and D-b-hydroxybutyrate. This occurs in severe, uncontrolled diabetes: because the tissues cannot use glucose, they oxidize large amounts of fatty acids instead. Although acetyl-CoA is not toxic, the mitochondrion must divert the acetyl-CoA to ketone bodies. What problem would arise if acetyl-CoA were not converted to ketone bodies? How does the diversion to ketone bodies solve the problem?
Chapter 9 Solutions
Biochemistry: The Molecular Basis of Life
Ch. 9 - Prob. 1QCh. 9 - Prob. 2QCh. 9 - Prob. 3QCh. 9 - Prob. 4QCh. 9 - Prob. 5QCh. 9 - Prob. 6QCh. 9 - Prob. 7QCh. 9 - Prob. 1RQCh. 9 - Prob. 2RQCh. 9 - Prob. 3RQ
Ch. 9 - Prob. 4RQCh. 9 - Prob. 5RQCh. 9 - Prob. 6RQCh. 9 - Prob. 7RQCh. 9 - Prob. 8RQCh. 9 - Prob. 9RQCh. 9 - Prob. 10RQCh. 9 - Prob. 11RQCh. 9 - Prob. 12RQCh. 9 - Prob. 13RQCh. 9 - Prob. 14RQCh. 9 - Prob. 15RQCh. 9 - Prob. 16RQCh. 9 - Prob. 17RQCh. 9 - Prob. 18RQCh. 9 - Prob. 19RQCh. 9 - Prob. 20RQCh. 9 - Prob. 21RQCh. 9 - Prob. 22RQCh. 9 - Prob. 23RQCh. 9 - Prob. 24RQCh. 9 - Prob. 25RQCh. 9 - Prob. 26RQCh. 9 - Prob. 27RQCh. 9 - Prob. 28FBCh. 9 - Prob. 29FBCh. 9 - Prob. 30FBCh. 9 - Prob. 31FBCh. 9 - Prob. 32FBCh. 9 - Prob. 33FBCh. 9 - Prob. 34FBCh. 9 - Prob. 35FBCh. 9 - Prob. 36FBCh. 9 - Prob. 37FBCh. 9 - Prob. 38SACh. 9 - Prob. 39SACh. 9 - Prob. 40SACh. 9 - Prob. 41SACh. 9 - Prob. 42SACh. 9 - Prob. 43TQCh. 9 - Prob. 44TQCh. 9 - Prob. 45TQCh. 9 - Prob. 46TQCh. 9 - Prob. 47TQCh. 9 - Prob. 48TQCh. 9 - Prob. 49TQCh. 9 - Prob. 50TQCh. 9 - Prob. 51TQCh. 9 - Prob. 52TQCh. 9 - Prob. 53TQCh. 9 - Prob. 54TQCh. 9 - Prob. 55TQCh. 9 - Prob. 56TQCh. 9 - Prob. 57TQCh. 9 - Prob. 58TQCh. 9 - Prob. 59TQ
Knowledge Booster
Learn more about
Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biochemistry and related others by exploring similar questions and additional content below.Similar questions
- When the acetyl-CoA produced during B-oxidation in the liver exceeds the capacity of the citric acid cycle, the excess acetyl-CoA forms ketone bodies-acetone, acetoacetate, and D-b-hydroxybutyrate. This occurs in severe, uncontrolled diabetes: because the tissues cannot use glucose, they oxidize large amounts of fatty acids instead. Although acetyl-CoA is not toxic, the mitochondrion must divert the acetyl-CoA to ketone bodies. What problem would arise if acetyl-CoA were not converted to ketone bodies? How does the diversion to ketone bodies solve the problem?arrow_forwardThe consumption of alcohol (ethanol), especially after periods of strenuous activity or after not eating for several hours, results in a deficiency of glucose in the blood, a condition known as hypoglycemia. The first step in the metabolism of ethanol by the liver is oxidation to acetaldehyde, catalyzedby liver alcohol dehydrogenase: Explain how this reaction inhibits the transformation of lactate to pyruvate. Why does this lead to hypoglycemia?arrow_forwardVon Gierke’s disease is also known as glycogen storage disease type I. Patients with von Gierke’s disease lackglucose 6-phosphatase activity. Two prominent symptoms of this disorder are fasting hypoglycemia and lactic acidosis (elevated lactate levels in the blood), especially during strenuous exercise. Explain why these symptoms occur. What chemical reaction does this enzyme catalyze? Which pathways involve this enzyme? Lacking thisthe enzyme will cause impairment of which pathways?• Pls consider what pathways are affected by Von Gierke’s disease. Include in your explanation involving Cori’s cycle. can you please do not write by your hand? I mean computer if you can. thank youarrow_forward
- Von Gierke’s disease is also known as glycogen storage disease type I. Patients with von Gierke’s disease lackglucose 6-phosphatase activity. Two prominent symptoms of this disorder are fasting hypoglycemia and lactic acidosis (elevated lactate levels in the blood), especially during strenuous exercise. Explain why these symptoms occur. What chemical reaction does this enzyme catalyze? Which pathways involve this enzyme? Lacking thisenzyme will cause impairment of which pathways?• Pls consider what pathways are affected by Von Gierke’s disease. Include in your explanation involving the Cori’s cycle.arrow_forwardWhich of the following are required to begin the citric acid cycle? (select all that apply) Group of answer choices pyruvate oxaloacetate Acetyl CoA glucose pyruvate dehydrogenase What are the 2 main types of mechanisms involved in regulating the activity of the pyruvate dehydrogenase complex in response to the state of the cell/organism? (select all that apply) Group of answer choices isomerization hydration allosteric regulation induced fit covalent modification Which of the following are likely to negatively regulate (decrease) the conversion of pyruvate to acetyl CoA? (select all that apply) Group of answer choices High levels of ATP Increased PDH kinase activity Influx of Ca2+ ions Insulin signaling High levels of NADHarrow_forwardFourteen NADPH molecules are required to produce one molecules of palmitic acid from acetyl CoA. Substantiate this statement by referring to the enzymatic activities involved in reduction steps during fatty acid synthesis and the number of cycles required to produce palmitic acid from acetyl CoA. How many molecules of ATP is required for the synthesis of palmitic acid from cytosolic acetyl-CoA?arrow_forward
- TPI deficiency is a rare human condition. Patients who lack TPI cannot convert the triose dihydroxyacetone phosphate into glyceraldehyde 3-phosphate.What happens to glycolysis in TPI patients?TPI patients suffer from chronic hemolytic anemia (abnormal breakdown of red blood cells) and have variable neuromuscular dysfunctions, including muscle weakness, poor muscle tone, and atrophy. Most die of respiratory failure during childhood. Explain why TPI-deficient patients exhibit these conditions using the diagram to justify your answer. TPI is enzyme 5.G6PD deficiency is one of the most common human genetic conditions, affecting about 40 million people worldwide. Patients suffer from hemolytic anemia when exposed to certain drugs, viral or bacterial disease, or fava beans.arrow_forwardPyruvate dehydrogenase kinase-4 (PDK-4) is a widely expressed isoform of PDK and is responsible for inhibiting pyruvate dehydrogenase (PDH) complex activity via phosphorylation. When PDK-4 is active, the PDH complex is in its phosphorylated state and pyruvate cannot be converted into acetyl-CoA for entry into the citric acid cycle. Instead, in gluconeogenic tissues like liver and kidney, pyruvate is channeled to support gluconeogenesis. Conversely, when PDK-4 is inactive, the PDH complex readily converts pyruvate into acetyl-CoA. A researcher wants to determine the role of PDK-4 on blood glucose homeostasis. To accomplish this, she proposes to generate a PDK-4 knockout mouse using CRISPR technology. To create the knockout mouse, she must first generate PDK-4 knockout embryos to implant into pseudopregnant female mice. Arrange the steps to outline the process by which she will generate the PDK-4 knockout embryos. First step Last step Answer Bank Generate Cas9 mRNA and sgRNA specific to…arrow_forwardEthanol is oxidized in the liver to form acetate, which is then converted to acetyl-CoA. Determine how many molecules of ATP are produced from 1 mol of ethanol. (Note that 2 mol of NADH are produced when ethanol is oxidized to form acetate.)arrow_forward
- Name three enzymes from the citric acid cycle which are allosterically regulated by ATP and/or NADH. Indicate if the binding of these effectors positively or negatively regulate the activity of each of these enzymesarrow_forwardThe citric acid cycle is a critical sequence of reactions for energy production, which take place in the matrix of the mitochondria. The reaction cycle requires materials from the cytosol to be converted into acetyl CoA, which represents the starting point of a new cycle. Which of the following statements about acetyl CoA is true? (a) Acetyl CoA is recycled at the end of every cycle. (b) Oxaloacetate is attached to acetyl CoA to feed the citric acid cycle. (c) Triacylglycerol molecules are transported into the mitochondrial matrix and cleaved by lipases to produce acetyl CoA. (d) Oxaloacetate is converted directly into acetyl CoA to feed the citric acid cyclearrow_forwardArsenate (HAsO42-) can replace inorganic phosphate (Pi) in the reaction catalyzed by glyceraldehyde 3-phosphate dehydrogenase, causing Glyceraldehyde 3-phosphate to be directly converted to 3-phosphoglycerate (NADH is still formed). If a cell is expose to Arsenate, which of the following metabolites of glycolysis will not be detectable in the cell? 2-phosphoglycerate 3-phosphoglycerate Fructose 6-phosphate Glucose 6-phosphate 1,3-bisphosphoglyceratearrow_forward
arrow_back_ios
SEE MORE QUESTIONS
arrow_forward_ios
Recommended textbooks for you
- BiochemistryBiochemistryISBN:9781319114671Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.Publisher:W. H. FreemanLehninger Principles of BiochemistryBiochemistryISBN:9781464126116Author:David L. Nelson, Michael M. CoxPublisher:W. H. FreemanFundamentals of Biochemistry: Life at the Molecul...BiochemistryISBN:9781118918401Author:Donald Voet, Judith G. Voet, Charlotte W. PrattPublisher:WILEY
- BiochemistryBiochemistryISBN:9781305961135Author:Mary K. Campbell, Shawn O. Farrell, Owen M. McDougalPublisher:Cengage LearningBiochemistryBiochemistryISBN:9781305577206Author:Reginald H. Garrett, Charles M. GrishamPublisher:Cengage LearningFundamentals of General, Organic, and Biological ...BiochemistryISBN:9780134015187Author:John E. McMurry, David S. Ballantine, Carl A. Hoeger, Virginia E. PetersonPublisher:PEARSON
Biochemistry
Biochemistry
ISBN:9781319114671
Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.
Publisher:W. H. Freeman
Lehninger Principles of Biochemistry
Biochemistry
ISBN:9781464126116
Author:David L. Nelson, Michael M. Cox
Publisher:W. H. Freeman
Fundamentals of Biochemistry: Life at the Molecul...
Biochemistry
ISBN:9781118918401
Author:Donald Voet, Judith G. Voet, Charlotte W. Pratt
Publisher:WILEY
Biochemistry
Biochemistry
ISBN:9781305961135
Author:Mary K. Campbell, Shawn O. Farrell, Owen M. McDougal
Publisher:Cengage Learning
Biochemistry
Biochemistry
ISBN:9781305577206
Author:Reginald H. Garrett, Charles M. Grisham
Publisher:Cengage Learning
Fundamentals of General, Organic, and Biological ...
Biochemistry
ISBN:9780134015187
Author:John E. McMurry, David S. Ballantine, Carl A. Hoeger, Virginia E. Peterson
Publisher:PEARSON
Anaerobic Respiration; Author: Bozeman Science;https://www.youtube.com/watch?v=cDC29iBxb3w;License: Standard YouTube License, CC-BY