Biochemistry: The Molecular Basis of Life
6th Edition
ISBN: 9780190209896
Author: Trudy McKee, James R. McKee
Publisher: Oxford University Press
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Chapter 8, Problem 6Q
Summary Introduction
To review:
The reasons why glucose always enter the cells in the phosphorylated form.
Introduction:
Glucose enters the cell and gets converted into pyruvate through sequential reactions, generating energy and this process is known as glycolysis. After that, pyruvate is oxidized to carbon dioxide and water, generating enormous amount of energy. Glucose generally comes from the diet, but in case of starvation, there are other precursors for glucose.
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Von Gierke’s disease is a rare genetic disorder that results in a deficiency of glucose-6-phosphatase. Symptoms ketoacidosis, a buildup of glycogen in the liver, and lactate buildup. Why does this glycogen storage disease not affect the brain?
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b) None of the above
c) In the event of hypoglycemia, the brain is able to utilize other sources of energy to produce ATP
d) The brain is able to metabolize lactate, which is present in high concetrations.
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Explain why triglycerides have a glucose-sparing effect.
Chapter 8 Solutions
Biochemistry: The Molecular Basis of Life
Ch. 8 - Prob. 1QCh. 8 - Prob. 2QCh. 8 - Prob. 3QCh. 8 - Prob. 4QCh. 8 - Prob. 5QCh. 8 - Prob. 6QCh. 8 - Prob. 7QCh. 8 - Prob. 1RQCh. 8 - Prob. 2RQCh. 8 - Prob. 3RQ
Ch. 8 - Prob. 4RQCh. 8 - Prob. 5RQCh. 8 - Prob. 6RQCh. 8 - Prob. 7RQCh. 8 - Prob. 8RQCh. 8 - Prob. 9RQCh. 8 - Prob. 10RQCh. 8 - Prob. 11RQCh. 8 - Prob. 12RQCh. 8 - Prob. 13RQCh. 8 - Prob. 14RQCh. 8 - Prob. 15RQCh. 8 - Prob. 16RQCh. 8 - Prob. 17RQCh. 8 - Prob. 18RQCh. 8 - Prob. 19RQCh. 8 - Prob. 20RQCh. 8 - Prob. 21RQCh. 8 - Prob. 22RQCh. 8 - Prob. 23RQCh. 8 - Prob. 24RQCh. 8 - Prob. 25RQCh. 8 - Prob. 26RQCh. 8 - Prob. 27RQCh. 8 - Prob. 28RQCh. 8 - Prob. 29RQCh. 8 - Prob. 30RQCh. 8 - Prob. 31RQCh. 8 - Prob. 32RQCh. 8 - Prob. 33RQCh. 8 - Prob. 34RQCh. 8 - Prob. 35RQCh. 8 - Prob. 36RQCh. 8 - Prob. 37RQCh. 8 - Prob. 38RQCh. 8 - Prob. 39RQCh. 8 - Prob. 40FBCh. 8 - Prob. 41FBCh. 8 - Prob. 42FBCh. 8 - Prob. 43FBCh. 8 - Prob. 44FBCh. 8 - Prob. 45FBCh. 8 - Prob. 46FBCh. 8 - Prob. 47FBCh. 8 - Prob. 48FBCh. 8 - Prob. 49FBCh. 8 - Prob. 50SACh. 8 - Prob. 51SACh. 8 - Prob. 52SACh. 8 - Prob. 53SACh. 8 - Prob. 54SACh. 8 - Prob. 55TQCh. 8 - Prob. 56TQCh. 8 - Prob. 57TQCh. 8 - Prob. 58TQCh. 8 - Prob. 59TQCh. 8 - Prob. 60TQCh. 8 - Prob. 61TQCh. 8 - Prob. 62TQCh. 8 - Prob. 63TQCh. 8 - Prob. 64TQCh. 8 - Prob. 65TQCh. 8 - Prob. 66TQCh. 8 - Prob. 67TQCh. 8 - Prob. 68TQCh. 8 - Prob. 69TQCh. 8 - Prob. 70TQCh. 8 - Prob. 71TQCh. 8 - Prob. 72TQCh. 8 - Prob. 73TQ
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Similar questions
- Glucagon is released from the pancreas in response to low blood glucose levels. It regulates the opposing pathways of glycolysis and gluconeogenesis by altering levels of fructose 2,6-bisphosphate. If glucagon causes a decrease in fructose 2,6-bisphosphate, how does this increase blood glucose levels? Explain..arrow_forwardHers disease results from an absence of liver glycogen phosphorylase and may result in serious illness. In McArdle disease, muscle glycogen phosphorylase is absent. Although exercise is difficult for patients suffering from McArdle disease, the disease is rarely life threatening. Account for the different manifestations of the absence of glycogen phosphorylase in the two tissues. What does the existence of these two different diseases indicate about the genetic nature of the phosphorylase?arrow_forwardThe “keto diet” is a dietary regimen in which carbohydrates are severely restricted, protein intake is low, and fat comprises 70–90% of daily calories. The diet causes “nutritional ketosis,” which is a different metabolic state than the ketosis that occurs in an untreated diabetic. The normal ketone body concentration is less than 0.6 mM. Explain why an individual on the keto diet may have a blood ketone body concentration of up to 3 mM. What biochemical pathways are active in an individual adhering to the keto diet? What pathways are largely inactive? Protein intake is kept low because a high-protein diet would inhibit ketosis. Explain why. Why might the keto diet lead to weight loss?arrow_forward
- Many patients with glucose 6- phosphatase deficiency have high serum levels of urate. Hyperuricemia can be induced in normal people by the ingestion of alcohol or by strenuous exercise. Propose a common mechanism that accounts for these findings.arrow_forwardWhy does the lack of glucose 6- phosphatase activity in the brain and muscle make good physiological sense?arrow_forwardwhat effect would an increase in glucose typically have on the activity of glycogen synthasearrow_forward
- Conversion of glucose 6-phosphate to glucose is done by the enzyme glucose 6-phosphatase which is present in the liver. identify any regulators to this process.arrow_forwardWrite a one-sentence explanation for each of the following statements. (a) In liver, glucagon stimulates glycogen breakdown via cyclic AMP. Although one might expect glucagon also to stimulate catabolism of the glucose formed, glucagon inhibits glycolysis and stimulates glu- coneogenesis in liver. (b) An individual with a glucose-6-phosphatase deficiency suffers from chronic hypoglycemia. (c) The action of phosphorylase kinase simultaneously activates glycogen breakdown and inhibits glycogen synthesis. (d) The presence in liver of glucose-6-phosphatase is essential to the function of the liver in synthesizing glucose for use by other tissues.arrow_forwardWhat are the effects of Glucose-6 Phosphate Dehydrogenase Deficiency? Explain its mechanism of action.arrow_forward
- Why are the enzymes α-Amylase and α-glucosidase active in a patient with hyperglycemia or diabetes? How do they become activated?arrow_forwardWhat would be the result of a lack of glucose 6-phosphatase activity?arrow_forwardGlucose 6-phosphatase deficiency is a glycogen storage disease referred to as von Gierke disease. Which of the following symptoms would you NOT expect to see in patients with this disease? (A) severe fasting hypoglycemia (B) excess adipose triglyceride storage and low circulating levels of fatty acids (C) hyperammonemia (D) liver enlargement resulting from excess liver glycogen storage (E) lactic acidosis (F) goutarrow_forward
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