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 16, Problem 47SA
Summary Introduction
To review:
The reason for linking adiponectin to the
Introduction:
Metabolic syndrome is the group of clinical disorders including dyslipidemia, hypertension, insulin resistance, and obesity. Insulin resistance originates because of the excess levels of FFA (free fatty acids) in the bloodstream.
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Students have asked these similar questions
Write 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.
Write a one-sentence explanation for each of the following statements.(a) In liver, glucagon stimulates glycogen breakdown via cAMP. Although you might expect glucagon to stimulate catabolism of the glucose formed as well, glucagon inhibits glycolysis and stimulates gluconeogenesis in liver.(b) An individual with a glucose-6-phosphatase deficiency suffers fromchronic hypoglycemia.(c) The action of phosphorylase kinase simultaneously activates glycogenbreakdown 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.
Mutations in glucokinase which lower the kcat for the enzyme or elevate the Km for glucose result in mild to moderate elevation of blood glucose. Explain how these mutations cause diabetes-like symptoms in patients.
Chapter 16 Solutions
Biochemistry: The Molecular Basis of Life
Ch. 16 - Prob. 1QCh. 16 - Prob. 2QCh. 16 - Prob. 3QCh. 16 - Prob. 4QCh. 16 - Prob. 5QCh. 16 - Prob. 6QCh. 16 - Prob. 7QCh. 16 - Prob. 8QCh. 16 - Prob. 1RQCh. 16 - Prob. 2RQ
Ch. 16 - Prob. 3RQCh. 16 - Prob. 4RQCh. 16 - Prob. 5RQCh. 16 - Prob. 6RQCh. 16 - Prob. 7RQCh. 16 - Prob. 8RQCh. 16 - Prob. 9RQCh. 16 - Prob. 10RQCh. 16 - Prob. 11RQCh. 16 - Prob. 12RQCh. 16 - Prob. 13RQCh. 16 - Prob. 14RQCh. 16 - Prob. 15RQCh. 16 - Prob. 16RQCh. 16 - Prob. 17RQCh. 16 - Prob. 18RQCh. 16 - Prob. 19RQCh. 16 - Prob. 20RQCh. 16 - Prob. 21RQCh. 16 - Prob. 22RQCh. 16 - Prob. 23RQCh. 16 - Prob. 24RQCh. 16 - Prob. 25RQCh. 16 - Prob. 26RQCh. 16 - Prob. 27RQCh. 16 - Prob. 28RQCh. 16 - Prob. 29RQCh. 16 - Prob. 30RQCh. 16 - Prob. 31RQCh. 16 - Prob. 32RQCh. 16 - Prob. 33RQCh. 16 - Prob. 34FBCh. 16 - Prob. 35FBCh. 16 - Prob. 36FBCh. 16 - Prob. 37FBCh. 16 - Prob. 38FBCh. 16 - Prob. 39FBCh. 16 - Prob. 40FBCh. 16 - Prob. 41FBCh. 16 - Prob. 42FBCh. 16 - Prob. 43FBCh. 16 - Prob. 44SACh. 16 - Prob. 45SACh. 16 - Prob. 46SACh. 16 - Prob. 47SACh. 16 - Prob. 48SACh. 16 - Prob. 49TQCh. 16 - Prob. 50TQCh. 16 - Prob. 51TQCh. 16 - Prob. 52TQCh. 16 - Prob. 53TQCh. 16 - Prob. 54TQCh. 16 - Prob. 55TQCh. 16 - Prob. 56TQCh. 16 - Prob. 57TQCh. 16 - Prob. 58TQCh. 16 - Prob. 59TQCh. 16 - Prob. 60TQCh. 16 - Prob. 61TQCh. 16 - Prob. 62TQCh. 16 - Prob. 63TQCh. 16 - Prob. 64TQCh. 16 - Prob. 65TQCh. 16 - Prob. 66TQCh. 16 - Prob. 67TQCh. 16 - Prob. 68TQCh. 16 - Prob. 69TQCh. 16 - Prob. 70TQCh. 16 - Prob. 71TQCh. 16 - Prob. 72TQCh. 16 - Prob. 73TQCh. 16 - Prob. 74TQCh. 16 - Prob. 75TQ
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- 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.arrow_forward(i) Diabetes Mellitus is a metabolic condition characterised by chronic hyperglycaemia, the laboratory diagnosis of which involves the estimation of blood glucose levels. Diabetes mellitus has often been described as a “metabolic nightmare”, since it could lead to several other metabolic abnormalities. Discuss how diabetes mellitus may be linked to these metabolic abnormalities. (ii) What laboratory assessments may be used to diagnose or monitor each condition, resulting from the metabolic consequences of diabetes mellitus as discussed in Question 1 above?arrow_forwardGlucocorticoids (GC) are stress hormones that modulate glucose homeostasis. One effect is to reduce glucose uptake from the bloodstream into skeletal muscle and adipose tissue, to increase the catabolism of expendable proteins in the skeletal muscle, and to increase gluconeogenesis in the liver. Why are these metabolic adaptations important during stressful situations, like fasting/starvation? Predict how the glucocorticoid cortisol will affect blood urea concentrations.arrow_forward
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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? a) The brain is able to still perform glycolysis effectively 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.arrow_forwardPatients with a form of early-onset diabetes were found to carry a variety of mutations reducing the function of the glucokinase (GK) enzyme. These patients are heterozygous for one of the mutations, and thus show only partial rather than complete loss of GK activity. Answer the following questions about these patients. 1. How would blood sugar levels likely be affected in GK-mutation patients? Briefly explain your choice (25 words or less) a. Higher than normal b. Normal C. Lower than normal d. Cannot predict based on the provided informationarrow_forwardTPI 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_forward
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