Deck 30: Integration of Metabolism

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Question
Mrs.Keller weighs 50 kg and is 1.5 m tall.This means she is considered:

A)Obese.
B)Overweight.
C)Normal.
D)Underweight.
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Question
Excess alcohol can impair fatty acid oxidation in the liver, thereby diverting fatty acids into triglyceride synthesis.The triglycerides are then exported as VLDL, or they stay in the liver, contributing to the development of fatty liver.This alcohol effect is mediated by:

A)Impaired gluconeogenesis.
B)Inhibition of lactate dehydrogenase by alcohol.
C)Depletion of NAD+.
D)Excessive formation of ketone bodies from alcohol.
E)Inhibition of the carnitine shuttle.
Question
A 52-year-old man with chronic alcoholism has a plasma lipid profile with increased very-low-density lipoprotein (VLDL).The mechanism that best explains the increase of VLDL in the blood of patients with chronic alcoholism is:

A)Impaired β-oxidation of fatty acids in the liver.
B)Reduced synthesis of apolipoprotein B-100.
C)Inactivation of capillary lipoprotein lipase.
D)Increased synthesis of glycerol-3-phosphate in adipose tissue.
E)Increased levels of apolipoprotein E receptors in the liver.
Question
After their absorption in the intestine, most nutrients go to the liver first, before they reach the systemic circulation.Of the following nutrients, which one does not go to the liver before being distributed to the rest of the body?

A)Vitamin E.
B)Inorganic ions such as sodium and potassium.
C)Fructose.
D)Amino acids.
E)Glucose.
Question
Hemoglobin A₁C measurement can be used to monitor diabetic patients.The unique advantage of this test is that:

A)It determines glucose tolerance rather than glucose concentration.
B)It is more selective for glucose than any other commonly used laboratory test.
C)It monitors the long-term control of blood glucose.
D)It is especially accurate in determining the blood glucose concentration.
E)It assesses not the effects of glucose but those of ketone bodies.
Question
The insulin level is reduced in many (although not all) diabetic patients.Adipocyte metabolism in these hypoinsulinemic patients is altered in the following ways, in comparison with normal subjects:

A)Glycerolphosphate-acyl transferase activity is lower, and triglyceride synthesis slows down.
B)Hormone-sensitive adipose tissue lipase activity is reduced, and more triglyceride is stored.
C)More glucose transporter 4 (GLUT-4) transporters are deployed in the plasma membrane.
D)Enhanced lipoprotein lipase (LPL) activity leads to hypotriglyceridemia.
E)The synthesis of ketone bodies by adipocytes is increased.
Question
A 200-meter run is powered by the production of adenosine triphosphate (ATP) mainly from:

A)b-Oxidation.
B)Creatine phosphate.
C)Anaerobic metabolism of glycogen.
D)Lactate obtained from the Cori cycle.
E)Glucose oxidation.
Question
You have been on a strict Atkins diet for the past 2 weeks.Of your calories, 80% come from fat, 15% from protein, and 5% from carbohydrate.What is the major source of blood glucose under these conditions?

A)Gluconeogenesis from amino acids.
B)Muscle glycogenolysis.
C)Gluconeogenesis from lactate.
D)Hepatic glycogenolysis.
E)Gluconeogenesis from acetyl-CoA.
Question
The susceptibility to type 1 diabetes is affected by genes.Genes that are especially important for susceptibility to type 1 diabetes are those coding for:

A)GLUT-4 transporters, which bring glucose into muscle and adipose tissue.
B)Human leukocyte antigens (HLA), which regulate immune responses.
C)The insulin receptor.
D)Glucokinase.
E)The nuclear receptor peroxisome proliferators-activated receptor (PPAR) , which is the target of glitazone drugs.
Question
In Type I diabetes, high levels of ketone bodies are liable to result in acidosis because:

A)The brain consumes very large amounts of acetoacetate.
B)The kidneys excrete large amounts of protonated ketone bodies.
C)The ketone bodies are acids, but the triglycerides from which they are formed are not.
D)Ketone bodies combine with circulating plasma bicarbonate.
E)Ketone bodies increase the urinary excretion of protons.
Question
Infectious illnesses can precipitate ketoacidosis in patients with insulin-dependent diabetes.The reason for this is:

A)Excessive formation of ketone bodies by cells of the immune system.
B)Reduced food intake by the ill patient.
C)Stimulation of lipolysis in adipose tissue by cortisol and epinephrine.
D)Impaired function of the insulin-secreting β cells during fever.
E)Excessive glycogen synthesis in response to cytokines.
Question
Acute ethanol intake raises the NADH/NAD⁺ ratio in the liver.This can inhibit gluconeogenesis by influencing the reaction catalyzed by:

A)Fructose-1-6-biphosphatase.
B)Glyceraldehyde-3-phosphate dehydrogenase.
C)Lactate dehydrogenase.
D)Phosphoenolpyruvate (PEP) carboxykinase.
E)Pyruvate carboxylase.
Question
You are treating a diabetic/hypertensive patient.When evaluating the effectiveness of the medical and dietary regimen, which of these results should give you reason for concern?

A)Fasting blood glucose: 100 mg/dL.
B)Glycosylated hemoglobin: 9%.
C)Blood pressure: 120/80.
D)Body mass index: 24.
E)Sodium intake: 3000 mg/day.
Question
One of the reasons for hyperglycemia in patients with diabetes mellitus is the effect of insulin on GLUT-4 transporters in:

A)All tissues.
B)Brain and erythrocytes.
C)Liver and adipose tissue.
D)Muscle and adipose tissue.
E)Liver and brain.
Question
When you wake up in the morning, 12 hours after supper, the main source of blood glucose is:

A)Dietary glucose from the intestine.
B)Muscle glycogen.
C)Gluconeogenesis from amino acids.
D)Liver glycogen.
E)Gluconeogenesis from glycerol.
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Deck 30: Integration of Metabolism
1
Mrs.Keller weighs 50 kg and is 1.5 m tall.This means she is considered:

A)Obese.
B)Overweight.
C)Normal.
D)Underweight.
Normal.
2
Excess alcohol can impair fatty acid oxidation in the liver, thereby diverting fatty acids into triglyceride synthesis.The triglycerides are then exported as VLDL, or they stay in the liver, contributing to the development of fatty liver.This alcohol effect is mediated by:

A)Impaired gluconeogenesis.
B)Inhibition of lactate dehydrogenase by alcohol.
C)Depletion of NAD+.
D)Excessive formation of ketone bodies from alcohol.
E)Inhibition of the carnitine shuttle.
Depletion of NAD+.
3
A 52-year-old man with chronic alcoholism has a plasma lipid profile with increased very-low-density lipoprotein (VLDL).The mechanism that best explains the increase of VLDL in the blood of patients with chronic alcoholism is:

A)Impaired β-oxidation of fatty acids in the liver.
B)Reduced synthesis of apolipoprotein B-100.
C)Inactivation of capillary lipoprotein lipase.
D)Increased synthesis of glycerol-3-phosphate in adipose tissue.
E)Increased levels of apolipoprotein E receptors in the liver.
Impaired β-oxidation of fatty acids in the liver.
4
After their absorption in the intestine, most nutrients go to the liver first, before they reach the systemic circulation.Of the following nutrients, which one does not go to the liver before being distributed to the rest of the body?

A)Vitamin E.
B)Inorganic ions such as sodium and potassium.
C)Fructose.
D)Amino acids.
E)Glucose.
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Unlock for access to all 15 flashcards in this deck.
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k this deck
5
Hemoglobin A₁C measurement can be used to monitor diabetic patients.The unique advantage of this test is that:

A)It determines glucose tolerance rather than glucose concentration.
B)It is more selective for glucose than any other commonly used laboratory test.
C)It monitors the long-term control of blood glucose.
D)It is especially accurate in determining the blood glucose concentration.
E)It assesses not the effects of glucose but those of ketone bodies.
Unlock Deck
Unlock for access to all 15 flashcards in this deck.
Unlock Deck
k this deck
6
The insulin level is reduced in many (although not all) diabetic patients.Adipocyte metabolism in these hypoinsulinemic patients is altered in the following ways, in comparison with normal subjects:

A)Glycerolphosphate-acyl transferase activity is lower, and triglyceride synthesis slows down.
B)Hormone-sensitive adipose tissue lipase activity is reduced, and more triglyceride is stored.
C)More glucose transporter 4 (GLUT-4) transporters are deployed in the plasma membrane.
D)Enhanced lipoprotein lipase (LPL) activity leads to hypotriglyceridemia.
E)The synthesis of ketone bodies by adipocytes is increased.
Unlock Deck
Unlock for access to all 15 flashcards in this deck.
Unlock Deck
k this deck
7
A 200-meter run is powered by the production of adenosine triphosphate (ATP) mainly from:

A)b-Oxidation.
B)Creatine phosphate.
C)Anaerobic metabolism of glycogen.
D)Lactate obtained from the Cori cycle.
E)Glucose oxidation.
Unlock Deck
Unlock for access to all 15 flashcards in this deck.
Unlock Deck
k this deck
8
You have been on a strict Atkins diet for the past 2 weeks.Of your calories, 80% come from fat, 15% from protein, and 5% from carbohydrate.What is the major source of blood glucose under these conditions?

A)Gluconeogenesis from amino acids.
B)Muscle glycogenolysis.
C)Gluconeogenesis from lactate.
D)Hepatic glycogenolysis.
E)Gluconeogenesis from acetyl-CoA.
Unlock Deck
Unlock for access to all 15 flashcards in this deck.
Unlock Deck
k this deck
9
The susceptibility to type 1 diabetes is affected by genes.Genes that are especially important for susceptibility to type 1 diabetes are those coding for:

A)GLUT-4 transporters, which bring glucose into muscle and adipose tissue.
B)Human leukocyte antigens (HLA), which regulate immune responses.
C)The insulin receptor.
D)Glucokinase.
E)The nuclear receptor peroxisome proliferators-activated receptor (PPAR) , which is the target of glitazone drugs.
Unlock Deck
Unlock for access to all 15 flashcards in this deck.
Unlock Deck
k this deck
10
In Type I diabetes, high levels of ketone bodies are liable to result in acidosis because:

A)The brain consumes very large amounts of acetoacetate.
B)The kidneys excrete large amounts of protonated ketone bodies.
C)The ketone bodies are acids, but the triglycerides from which they are formed are not.
D)Ketone bodies combine with circulating plasma bicarbonate.
E)Ketone bodies increase the urinary excretion of protons.
Unlock Deck
Unlock for access to all 15 flashcards in this deck.
Unlock Deck
k this deck
11
Infectious illnesses can precipitate ketoacidosis in patients with insulin-dependent diabetes.The reason for this is:

A)Excessive formation of ketone bodies by cells of the immune system.
B)Reduced food intake by the ill patient.
C)Stimulation of lipolysis in adipose tissue by cortisol and epinephrine.
D)Impaired function of the insulin-secreting β cells during fever.
E)Excessive glycogen synthesis in response to cytokines.
Unlock Deck
Unlock for access to all 15 flashcards in this deck.
Unlock Deck
k this deck
12
Acute ethanol intake raises the NADH/NAD⁺ ratio in the liver.This can inhibit gluconeogenesis by influencing the reaction catalyzed by:

A)Fructose-1-6-biphosphatase.
B)Glyceraldehyde-3-phosphate dehydrogenase.
C)Lactate dehydrogenase.
D)Phosphoenolpyruvate (PEP) carboxykinase.
E)Pyruvate carboxylase.
Unlock Deck
Unlock for access to all 15 flashcards in this deck.
Unlock Deck
k this deck
13
You are treating a diabetic/hypertensive patient.When evaluating the effectiveness of the medical and dietary regimen, which of these results should give you reason for concern?

A)Fasting blood glucose: 100 mg/dL.
B)Glycosylated hemoglobin: 9%.
C)Blood pressure: 120/80.
D)Body mass index: 24.
E)Sodium intake: 3000 mg/day.
Unlock Deck
Unlock for access to all 15 flashcards in this deck.
Unlock Deck
k this deck
14
One of the reasons for hyperglycemia in patients with diabetes mellitus is the effect of insulin on GLUT-4 transporters in:

A)All tissues.
B)Brain and erythrocytes.
C)Liver and adipose tissue.
D)Muscle and adipose tissue.
E)Liver and brain.
Unlock Deck
Unlock for access to all 15 flashcards in this deck.
Unlock Deck
k this deck
15
When you wake up in the morning, 12 hours after supper, the main source of blood glucose is:

A)Dietary glucose from the intestine.
B)Muscle glycogen.
C)Gluconeogenesis from amino acids.
D)Liver glycogen.
E)Gluconeogenesis from glycerol.
Unlock Deck
Unlock for access to all 15 flashcards in this deck.
Unlock Deck
k this deck
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Unlock Deck
Unlock for access to all 15 flashcards in this deck.