1/117
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai |
|---|
No analytics yet
Send a link to your students to track their progress
Why do lipoproteins (e.g. VLDL) only have a monolayer of phospholipids instead of a typical lipid bilayer?
A. The phosphate of the lipids interact with the triglycerides and cholesterol esters of the particle.
B. The monolayer protects the particles from bile acids
C. The acyl chains of the phospholipid monolayer interact with the triglycerides and cholesterol esters of the particle.
D. The glycerol backbone solubilize the triglycerides
E. The monolayer blocks proteases from degrading the particles
C. The acyl chains of the phospholipid monolayer interact with triglycerides and cholesterol esters of the particle
Odd chain fatty acids and some amino acids produce propionyl CoA. Which of the following is NOT required for the metabolism of propionyl CoA to succinyl CoA
A. NADH
B. Propionyl CoA carboxylase
C. Methylmalonyl CoA mutase
D. Vitamin B12
E. Biotin
NADH
Human can convert cholesterol to each of the following, except;
A. CO2 + H2O
B. Cortisol
C. Testosterone
D. Estradiol
E. Bile acids
CO2 and H20
Mammalian pyruvate dehydrogenase component E1 is inactivated through phosphorylation in the presence of _______?
A. High ADP
B. High pyruvate
C. Insulin
D. High Acetyl-CoA
E. High AMP
D. High Acetyl-CoA
Lovastatin is used to lower cholesterol by inhibiting the function of which protein?
A. HMG-CoA reductase
B. LDL receptor
C. Lipoprotein lipase
D. Cyclooxygenase
E. Alcohol dehydrogenase
A. HMG-CoA reductase
During vigorous exercise, stimulation of the tricarboxylic acid (TCA) cycle results principally from _____?
A. Allosteric activation of a number of TCA cycle enzymes by increased levels of NADH
B. Allosteric activation of fumarase by increased cellular ADP concentrations
C. Stimulation of the flux through a number of TCA cycle enzymes by a decreased NADH/NAD+ ratio
D. A rapid decrease in the concentration of four carbon intermediates being used by other metabolic pathways, e.g. gluconeogenesis
E. Product inhibition of the citrate synthase enzyme, which blocks the condensation of Acetyl CoA and oxaloacetate
C. Stimulation of the flux through a number of TCA cycle enzymes by a decreased NADH/NAD+ ratio
Triacylglycerol synthesis in adipose tissue occurs only in the fed state. Why?
A. Coenzyme A being required to activate the fatty acids prior to coupling to glycerol-3 phosphate
B. Lipoprotein lipase being activated only in the fed state by Apo-CII
C. Fatty acid for triacylglycerol synthesis being obtained from chylomicrons and VLDL, which is high in concentration after a meal with high fat content
D. Adipose tissue lacks glycerol kinase to make glycerol-3-phosphate from glycerol. Therefore, Glycerol-3-phosphate can only be obtained from the glycolytic pathway (fed state), and the reduction of dihydroxyacetone phosphate (DHAP)
E. None of the above.
D. Adipose tissue lacks glycerol kinase to make glycerol-3-phosphate from glycerol. Therefore, Glycerol 3-phosphate can only be obtained from the glycolytic pathway (fed state) and the reduction of DHAP
A patient with a genetic defect in lipoprotein lipase would be expected to exhibit which of the following?
A. A deficiency in release of fatty acids from adipocytes during fasting
B. Elevated glucose in fasting blood samples
C. Elevated intestinal absorption of fats
D. Elevated chylomicrons in fasting blood samples
E. Decreasing recycling of bile salts
D. Elevated chylomicrons in fasting blood samples
Suppose 14-C labeled CO2 is used to form malonyl CoA from acetyl CoA. if this labeled malonyl CoA is used for palmitate synthesis, which carbons in the fatty acid would be radiolabeled?
A. The methyl terminal carbon
B. Only the alpha and beta-carbons
C. All odd numbered carbons
D. All even numbered carbons
E. None of the carbons
E. none of the carbons
Fatty acids are adenylated prior to reacting with Coenzyme A to make Acyl-CoA. What is the purpose of the adenylation?
A. This creates a phospho-ester bond that can be "attacked" by Coenzyme A
B. Adenylation prevents Acyl-CoA from interacting with coenzyme A
C. Adenylation leads to the addition of ATP to the acyl chains
D. This allows for the growth of acyl chain length
E. All of the above
A. this creates a phospho ester bond that can be attacked by Coenzyme A
The carnitine derivatives of fatty acids are utilized for
A. Carrying fatty acids during fatty acid synthesis
B. Shuttling fatty acids across the mitochondrial membrane
C. One of the intermediates during beta-oxidation
D. Transporting fatty acids across the plasma membrane of the cell
E. Transporting fatty acids in plasma
B. Shuttling fatty acids across the mitochondrial membrane
Which of the following compounds is a potent stimulator of palmitate synthesis, an allosteric activator of acetyl-CoA carboxylase, and a source of both cytoplasmic acetyl-CoA and NADPH for lipogenesis?
A. Biotin
B. Glucose 6-phosphate
C. Citrate
D. Pantothenic acid
E. L-carnitine
C. Citrate
Which of the following is responsible for down regulation of fatty acid synthesis under low energy conditions?
A. Release of ATP inhibition of carnitine acyl transferase I
B. AMP activation of AMP activated protein kinase (AMPK)
C. AMP activation of PFK-1
D. AMP activation of PEP carboxykinase
E. Release of ATP inhibition of acetyl CoA carboxylase
B. AMP activation of AMP activated protein kinase (AMPK)
When fatty acid biosynthesis is stimulated, beta oxidation of fatty acids is inhibited. This inhibition occurs mainly because:*
A. High levels of ATP inhibit AMPK, which prevents acetyl CoA carboxylase 1 from being phosphorylated, keeping synthesis "on"
B. Acetyl-CoA activates pyruvate carboxylase
C. High levels of ATP inhibit phosphofructokinase
D. Malonyl-CoA inhibits carnitine acyltransferase I
E. The pool of acetyl-CoA is depleted by the TCA cycle and fatty acid biosynthesis
D. Malonyl CoA inhibits carnitine acyltransferase I
Which of the following statements about chylomicrons is incorrect?
A. Chylomicrons contain phospholipid
B. Lipoprotein lipase hydrolyzes triacylglycerols in chylomicrons
C. Chylomicrons travel initially through the lymphatic system before reaching the blood
D. Intestinal mucosal cells secrete chylomicrons
E. The main role of chylomicrons is to deliver cholesterol to the tissues and fatty acids to the liver.
E. The main role of chylomicrons is to deliver cholesterol to the tissues and fatty acids to the liver
Why is it important for biotin to be linked to the flexible arm of pyruvate carboxylase?
A. The biotin needs to move between the separated biotin carboxylation and carboxyltransferase sites within the same copy of the protein
B. The biotin needs to move between the separated biotin carboxylation and carboxyltransferase sites between adjacent copies of the protein in a tetramer
C. The biotin needs to move between the separated biotin carboxylation and carboxyltransferase sites between adjacent copies of the protein in a trimer
D. The biotin needs to move between the separated bitcoin decarboxylation and carboxyltransferase sites within the same copy of the protein.
E. The biotin needs to move between the separate biotin carboxylation and carboxyltransferase sites between adjacent copies of the protein in a dimer
B. the biotin needs to move between the seperated biotin carboxylation and carboxyltransferase sites between adjacent copies of the protein in a tetramer
What is the role of Carnitine acyltransferase-I?
A. Transport acyl chains into the mitochondrial matrix
B. Reacts with Acyl-CoA and L-carnitine to transfer the acyl chain to make Acyl-carnitine
C. Reacts with Acyl-carnitine and CoA to transfer the acyl chain to make Acyl-CoA
D. Reacts with Acyl-carnitine and CoA to transfer the acyl chain to make Acyl-CoA and transport Acyl chains into the mitochondrial matrix
E. Reacts with Acyl-CoA and L-Carnitine to transfer the acyl chain to make Acyl-carnitine and transport Acyl chains into the mitochondrial matrix
E. Reacts with Acyl-CoA and L-Carnitine to transfer the acyl chain to make Acyl-carnitine and transport Acyl chains into the mitochondrial matrix
Prior to removal of an Acetyl-CoA in Beta-oxidation, the saturated Beta carbon must be __________
A. Oxidized, hydrated, and dehydrated again to form L-3-hydroxyacyl CoA
B. Oxidized, dehydrated, and oxidized again to form trans-delta2-Enoyl CoA
C. Reduced, dehydrated, and reduced again to form butyryl ACP
D. Oxidized, hydrated, and oxidized again to form 3-ketoacyl CoA
E. Reduced, dehydrated, and reduced again to form D-3-hydroxybutyryl ACP
D. Oxidized, hydrated, and oxidized again to form 3-ketoacyl CoA
Which of the following is NOT true about fatty acid synthesis?
A. Intermediates are linked to acyl carrier proteins
B. Fatty acid synthesis occurs in the mitochondria
C. Intermediates are linked to acyl carrier proteins and fatty acid synthesis occurs in the mitochondria
D. Fatty acid synthesis occurs in the mitochondria and the coenzyme for the oxidation and reduction reactions in NADP+/NADPH
E. The coenzyme for the oxidation and reduction reactions is NADP+/NADPH
B. Fatty acid synthesis occurs in the mitochondria
What is the role of Biotin in beta oxidation of ODD chain carbon fatty acids?
A. Biotin adds CoA to odd-carbon acyl chain
B. Biotin removes CO2 from the odd-carbon chain
C. Biotin takes part in the addition of a CO2 to Propionyl-CoA
D. Biotin removes the terminal carbon to make an even-carbon chain
E. Biotin removes phosphate from ATP to form carboxyphosphate
C. Biotin takes part in the addition of a CO2 to Propionyl-CoA
Coenzyme A and acyl carrier protein (ACP) resemble one another since both
A. Contain biotin
B. Carry fatty acids across the mitochondrial membrane
C. Contain lipoic acid
D. Contain 4'-phosphopantetheine
E. None of these
D. Contain 4-phospopantetheine
Beta oxidation of fatty acids with even numbers of carbons will produce all of the following EXCEPT
A. FADH2
B. Malonyl-CoA
C. Butyryl-CoA
D. NADH
E. Acetyl-CoA
C. Butyrl-CoA
The end product of glycolysis is pyruvate. However, pyruvate cannot directly enter the TCA cycle. What needs to happen to pyruvate for the TCA cycle to proceed?
A. Pyruvate must lose a CO2 when it reacts with TPP and form hydroxyethyl-TPP and CoA-SH acquires an acetyl group to make Acetyl-CoA
B. Pyruvate must lose a CO2 when it reacts with TPP and form hydroxyethyl-TPP
C. Pyruvate must lose a CO2 when it reacts with TPP and form hydroxyethyl-TPP, the acetyl group linked to TPP must be transferred to lipoamide and CoA-SH acquires an acetyl group to make Acetyl-CoA
D. CoA-SH acquires an acetyl group to make Acetyl-CoA
E. The acetyl group linked to TPP must be transferred to lipoamide
C. Pyruvate must lose a CO2 when it reacts with TPP and form hydroxyethyl-TPP, the acetyl group linked to TPP must be transferred to lipoamide and CoA-SH acquires an acetyl group to make Acetyl-CoA
In gluconeogenesis the role of pyruvate kinases (in glycolysis) is replaced by what activities?
A. Production of phosphophenolpyruvate from oxaloacetate
B. Production of phosphophenolpyruvate from pyruvate and conversion of pyruvate to oxaloacetate by pyruvate carboxylase
C. Production of phosphophenolpyruvate from pyruvate
D. Conversion of pyruvate to oxaloacetate by pyruvate carboxylase and production of phosphoenolpyruvate from oxaloacetate.
E. Conversion of pyruvate to oxaloacetate by pyruvate carboxylase
D. Conversion of pyruvate to oxaloacetate by pyruvate carboxylase and production of phosphoenolpyruvate from oxaloacetate
Which is TRUE of the reciprocal regulation of glycolysis and gluconeogenesis?
A. ADP inhibits pyruvate carboxylase and activates pyruvate kinase, ATP inhibits phosphofructokinase and ATP activates fructose 1,6 biphosphatase
B. ADP inhibits pyruvate carboxylase and activates pyruvate kinase
C. ATP inhibits phosphofructokinase and ATP activates fructose 1,6 biphosphatase
D. Citrate inhibits fructose 1,6 biphosphatase and phosphofructokinase
E. Citrate inhibits fructose 1,6 biphosphatase and phosphofructokinase, ADP inhibits pyruvate carboxylase and ADP activates pyruvate kinase
A. ADP inhibits pyruvate carboxylase and activates pyruvate kinase, ATP inhibits phosphofructokinase and ATP activates fructose 1,6 biphosphatase
What is the effect of Protein kinase A phosphorylation of Fructose 2,6-bisphosphate?
A. Inhibits fructose 2,6 bisphosphatase kinase domain
B. Activates the fructose 2,6, bisphosphatase kinase domain
C. Activates fructose 1,6 bisphosphatase
D. Inhibits both fructose 2,6 bisphosphatase domain and kinase domain
E. Increases glucagon signaling
A. Inhibits fructose 2,6 bisphosphatase kinase domain
What is the role of Adenylate cyclase in gluconeogenesis?
A. It converts cAMP to AMP, which activates PKA
B. Converts ATP to cAMP, which activates PKA
C. Converts AMP to cADP which inhibits PKA
D. Converts ATP to cAMP which inhibits PKA
E. Converts cAMP to AMP which inhibits PKA
B. Converts ATP to cAMP, which activates PKA
The Aconitase reaction of the TCA results in moving a C3-OH to the C2 position. How does this facilitate the isocitrate lyase reaction?
A. The new carbonyl at C3 allows for binding Mg2+ along with C1-carboxylate
B. Allows for C2 decarboxylation
C. Allows for C3 dehydration
D. Allows for C2 decarboxylation and the new carbonyl at C3
allows for binding Mg2+ along with C1-carboxylate
E. Allows for C2 decarboxylation als allows for C3 dehydration
D. Allows for C2 decarboxylation and the new carbonyl at C3
allows for binding Mg2+ along with C1-carboxylate
What happens when fumarate is reduced?
A. It gains 1 H+ and 1 e- to make succinate
B. It severs the alkene bond of fumarate
C. It loses 2H+ to make oxaloacetate
D. It gains 2H+ and 2 e- to make succinate
E. It gains 2 H+ and 2 e- to make oxaloacetate
D. It gains 2H+ and 2 e- to make succinate
Cytosolic Ca2+ plays an important role during glycogen synthesis. What leads to an increase in cytosolic Ca2+?
A. Phospholipase-C is activated, which cleaves PI(4,5)P2 to release IP3, IP3 binds to a specific receptor on the endoplasmic reticulum, which triggers the release of Ca2+ into the cytoplasm.
B. Phospholipase-E is activated, which cleaves PI(4,5)P2 to release IP4,5. IP4,5 binds to a specific receptor on the endoplasmic reticulum, which triggers the release of Ca2+ into the cytoplasm.
C. Phospholipase-C is activated, which cleaves PI(4,5)P2 to release soluble DAG. DAG binds to a specific receptor on the endoplasmic reticulum, which triggers the release of Ca2+ into the cytoplasm.
D. Phospholipase D is activated, which cleaves PI(3,4,5)P2 to release IP3. IP3 binds to a specific receptor on the endoplasmic reticulum, which triggers the release of Ca2+ into the cytoplasm.
E. Ca2+ does not play a role in glycogen synthase
B. Phospholipase-E is activated, which cleaves PI(4,5)P2 to release IP4,5. IP4,5 binds to a specific receptor on the endoplasmic reticulum, which triggers the release of Ca2+ into the cytoplasm.
How does arsenite poisoning take effect?
A. Arsenite prevents the oxidation of reduced lipoyllysine
B. Arsenite covalently attached to dihydrolipoamide and prevents pyruvate processing to acetyl-CoA
C. Arsenite prevents competes for pyruvate reacting with the TPP of E1 it the pyruvate dehydrogenase complex
D. Arsenite blocks the reaction of acetyl-CoA and oxaloacetate to form citrate
E. All of the above
B. Arsenite covalently attached to dihydrolipoamide and prevents pyruvate processing to acetyl-CoA
Which of the following coenzymes are used by alpha ketoglutarate dehydrogenase complex?
A. Lipoic acid
B. CoA
C. FAD and NAD+
D. All of the above
D. all of the above
During cholesterol synthesis how is C-30 squalene made?
A. The oxidation of 30-carbon lanosterol
B. Successive condensations of 10 3-carbon malonil units
C. Successive condensation of Six 5 carbon Isoprene molecules
D. Successive condensations of Six 5-carbon mevalonate units
E. Successive condensations of Five 6-carbon isoprene units
C. Successive condensation of Six 5 carbon Isoprene molecules
How can excess bile acids be reduced?
A. Decrease fructose in diet
B. Taking cholestyramine
C. Increase dietary fiber in diet
D. Increase dietary fiber in diet and taking cholestyramine
E. Increase dietary fiber in diet and decrease fructose in diet
D. Increase dietary fiber in diet and taking cholestyramine
What is true about omega fatty acids?
A. The omega number is independent of the length of the fatty acid
B. The omega number is independent of the length of the fatty acid and the omega number indicates where the first double bond is relative to the carboxylate
C. The omega number indicates where the first double bond is relative to the carboxylate
D. The omega number is independent of the length of the fatty acid and the omega number (e.g. Omega-3) indicates where the first double bond is relative to the final carbon in the fatty acid
E. The omega number (e.g. Omega-3) indicates where the first double bond is relative to the final carbon in the fatty acid
D. The omega number is independent of the length of the fatty acid and the omega number (e.g. Omega-3) indicates where the first double bond is relative to the final carbon in the fatty acid
Which is the CORRECT pairing of a tissue with its main fuel source is STARVATION?
A. Skeletal muscle--fatty acids
B. Brain--fatty acids
C. Adipose tissue--glucose
D. Liver--glucose
E. Erythrocytes--ketone bodies
D. Liver--glucose
A student celebrates by drinking alcoholic beverages during his entire 2 week vacation without eating any other foods. The celebration culminates with a loss of consciousness and a trip to the emergency room. The physical examination shows deep, rapid ventilation. The laboratory examination shows severe hypoglycemia and high levels of ketone bodies. These changes occurred because:
A. the severe muscle proteolysis and oxidation of branched chain amino acids to provide carbon skeletons for gluconeogenesis generated amino nitrogen in excess of the liver's capacity to detoxify it, leading to coma
B. Alcohol has little to do with this clinical picture. The lack of food caused glycogen stores to be used up after 1 to 2 weeks, producing hypoglycemia and fatty acid mobilization, with resultant ketone body synthesis
C.Alcohol is converted by the cytochrome P450 system to ketones and inhibits glucose-6-phosphatase in the liver so that the liver cannot release glucose into circulation
D. Alcohol, oxidized by alcohol dehydrogenase, depleted NAD while forming NADH, a situation inhibitory to gluconeogenesis. With no food to replenish glycogen, hypoglycemia ensued with a compensatory increase in fatty acid oxidation leading to the alcoholic ketosis
E. Alcohol enhances skeletal muscle uptake and utilization of glucose, leaving only fate (converted to ketone bodies in the liver) as an energy source for other organs
D. Alcohol, oxidized by alcohol dehydrogenase, depleted NAD while forming NADH, a situation inhibitory to gluconeogenesis. With no food to replenish glycogen, hypoglycemia ensued with a compensatory increase in fatty acid oxidation leading to the alcoholic ketosis
Alcohol abuse is a frequent cause of liver disease in the USA. in recent years, many attempts have been made to help alcoholics stop drinking. Disulfiram is one of the potential pharmacological approaches for preventing alcoholics from drinking. What is the name of the enzyme that is targeted by disulfiram?
A. Acetaldehyde dehydrogenase
B. Acetyl CoA synthetase
C. Cytochrome P450 2E1
D. Cytochrome P450 reductase
E. Alcohol dehydrogenase
A. Acetaldehyde dehydrogenase
Mammalian pyruvate dehydrogenase component E1 is inactivated through phosphorylation in the presence of ___________
A. High pyruvate
B. Insulin
C. High acetyl-CoA
D. High AMP
E. High ADP
C. High acetyl-CoA
Brian Cooper, a 35-year-old business man, led a stressful life and didn't exercise. He ate irregularly, smoked, and drank, his physician suspected a heart problem and had tests performed to aid in the diagnosis. Elevated serum levels of low-density lipoproteins (LDL) are indicative of elevated levels of
A. Triacylglycerols
B. Lipoprotein lipase
C. HDL
D. Cholesterol
E. Chylomicrons
D. cholesterol
Lovastatin was used to treat Brian Cooper. The drug lovastatin works by inhibiting the function of which protein?
A. HMG-CoA reductase
B. Lipoprotein lipase
C. Cyclooxygenase
D. LDL receptor
E. Alcohol dehydrogenase
A. HMG-CoA reductase
A female is admitted to the Emergency Department, suffering from nausea and vomiting. Her blood work shows elevated liver enzymes in the blood and highly elevated acetaminophen levels. She is diagnosed with acetaminophen overdose. In acetaminophen toxicity, which of the following compounds is a toxic intermediate?
A. Acetaminophen glutathione
B. Acetaminophen sulfate
C. N-acetyl-p-benzoquinoneimine (NAPQI)
D. Acetaminophen glucuronide
E. N-acetyl-p-aminophenol
C. N-acetyl-p-benzoquinoneimine (NAPQI)
Which is TRUE of the reciprocal regulation of glycolysis and gluconeogenesis?
A. Citrate inhibits fructose-1,6-bisphosphatase and inhibits phosphofructokinase. ADP inhibits pyruvate carboxylase and activates pyruvate kinase
B. ADP inhibits pyruvate carboxylase and activates pyruvate kinase
C. Citrate inhibits fructose-1,6-bisphosphatase and inhibits phosphofructokinase
D. ATP inhibits phosphofructokinase and activates fructose-1,6-bisphosphatase
E. ADP inhibits pyruvate carboxylase and activates pyruvate kinase. ATP inhibits phosphofructokinase and activates fructose-1,6-bisphosphatase
E. ADP inhibits pyruvate carboxylase and activates pyruvate kinase. ATP inhibits phosphofructokinase and activates fructose-1,6-bisphosphatase
Chronic alcohol results in induction of Cytochrome P450 2E1 (CYP2E1) enzyme in the liver. Although the induction is a compensatory mechanism to metabolize excess alcohol, it can have negative consequences BECAUSE it
A. Leads to faster acetate production than can be cleared
B. Uses up most of the NADH available in the hepatocyte
C. Leads to production of formaldehyde, which causes ocular toxicity
D. Squelches the free radicals that protect against liver injury
E. Leads to faster acetaldehyde production than can be cleared
E. Leads to faster acetaldehyde production than can be cleared
A 20-year-old woman with type 1 diabetes was admitted to the hospital in a semi-conscious condition fever, nausea and vomiting. The woman's breath smelled of acetone. A urine sample was strongly positive for ketone bodies. In this patient:
a. The patient should be given an intravenous infusion of glucose to regain consciousness.
b. A blood glucose test would likely show that her blood glucose was well below 80 mg/dL.
c. The acetone must have been produced by spontaneous decarboxylation of β-hydroxybutyrate.
d. An insulin injection would alleviate her ketoacidosis by decreasing ketone body production.
e. Glucagon should be administered immediately to stimulate glycogenolysis and gluconeogenesis in the liver.
d. An insulin injection would alleviate her ketoacidosis by decreasing ketone body production.
During vigorous exercise, stimulation of the tricarboxylic acid (TCA) cycle results principally from _____?
A. Allosteric activation of a number of TCA cycle enzymes by increased levels of NADH
B. Allosteric activation of fumarase by increased cellular ADP concentrations
C. Stimulation of the flux through a number of TCA cycle enzymes by a decreased NADH/NAD+ ratio
D. A rapid decrease in the concentration of four carbon intermediates being used by other metabolic pathways, e.g. gluconeogenesis
E. Product inhibition of the citrate synthase enzyme, which blocks the condensation of Acetyl CoA and oxaloacetate
C. Stimulation of the flux through a number of TCA cycle enzymes by a decreased NADH/NAD+ ratio
Triacylglycerol synthesis in adipose tissue occurs only in the fed state. It is due to
A. Coenzyme A being required to activate the fatty acids prior to coupling to glycerol-3-phosphate.
B. Fatty acid for triacylglycerol synthesis being obtained from chylomicrons and VLDL, which is high in concentration after a meal with high fat content.
C. Lipoprotein lipase being activated only in the fed state by Apo-CII
D. The lack of glycerol kinases in adipose tissue that generates glycerol-3-phosphate is obtained from the glycolytic pathway operated in the fed state with high glucose concentration.
D. The lack of glycerol kinases in adipose tissue that generates glycerol-3-phosphate is obtained from the glycolytic pathway operated in the fed state with high glucose concentration
Tangier disease is characterized by a severe plasma deficiency or absences of HDL by accumulation of cholesterol esters in many tissues throughout the body. Which of the following proteins or enzymes is deficient in this condition?
A. Hepatic triglyceride lipase
B. Lipoprotein lipase
C. ABCA1 (ATP binding cassette protein 1)
D. ApoB 100
E. LDL receptor
ABCA1 (ATP binding cassette protein 1)
A patient with a genetic defect in lipoprotein lipase would be expected to exhibit which of the following?
A. Decreased intestinal absorption of fats
B. Decreased recycling of bile salts
C. Elevated chylomicrons in fasting blood samples
D. A deficiency in release of fatty acids from adipocytes during fasting
E. Elevated glucose in fasting blood samples
C. Elevated chylomicrons in fasting blood samples
A 6 month old boy was hospitalized following a seizure. History revealed that for several days prior his appetite was decreased due to a "stomach virus" at admission his blood glucose was 24 mg/dl (normal is 60-100 mg/dl) his urine was negative for ketone bodies but positive for a variety of dicarboxylic acids. A tentative diagnosis of medium-chain fatty acyl CoA dehydrogenase (MCAD) deficiency is made. In patients with MCAD deficiency the fasting hypoglycemia is a consequence of
A. Increased production of ATP and NADH
B. Decreased ability to convert acetyl CoA to glucose
C. Increased conversion of acetyl CoA to acetoacetate
D. Hemolytic anemia
E. Decreased acetyl CoA production
E. Decreased acetyl CoA production
Fatty acids are adenylated prior to reacting with CoA to make acyl CoA. What is the purpose of the adenylation?
A. This creates a phosphoester bond that can "attacked" by CoA
B. Adenylation leads to the addition of ATP to acyl chain length
C. This allows for the growth of acyl chain length
D. Adenylation prevents acyl CoA from interacting with CoA
E. All of the above
A. This creates a phosphoester bond that can "attacked" by CoA
In Gluconeogenesis aldolase functions to convert one glyceraldehyde 3-phosphate and one dihydroxyacetone phosphate to the following products
A. 1 DHAP and 1 enediolate
B. Fructose 1,6 bisphosphate
C. Fructose 2, 6 bisphosphate
D. Two glyceraldehyde 3 phosphate
E. Fructose 6 phosphate
B. Fructose 1,6 bisphosphate
A 40 year old homeless male is brought to the emergency department with confusion, shortness of breath and swelling of his leg. He is known to be an alcoholic and eats poorly, only canned soup and junk food in the homeless shelter. Physical examination indicates compromised left ventricular cardiac contractility. A simple blood test shows no ketoacidosis. What will be the most likely diagnosis?
A. Polycystic kidney disease due to chronic alcoholism, resulting in fluid retention
B. Early on-set of Parkinson's disease due to chronic alcoholism
C. Acute alcoholism with cardiac damage
D. Type 1 diabetes mellitus
E. Wet beri-beri caused by nutritional deficiency in vitamin B1
E. Wet beri-beri caused by nutritional deficiency in vitamin B1
A 35-year-old woman was seen in the emergency room because of recurrent abdominal pain. The history revealed a 2-year pattern of pain in the upper rightquadrant, beginning several hours after the ingestion of a meal rich in fried/fatty food. Ultrasonographic examination demonstrated the presence of numerous stones in the gallbladder. The patient initially elected treatment consisting of exogenously supplied chenodeoxycholic acid (a bile acid), but eventually underwent surgery for the removal of the gallbladder, and had a full recovery. The rationale for the initial treatment of this patient with chenodeoxycholic acid is that this compound:
A. increases cholesterol solubility in bile.
B. interferes with the enterohepatic circulation.
C. increases de novo bile acid production.
D. Inhibits cholesterol synthesis
E. stimulated VLDL production by the liver
A. increases cholesterol solubility in bile.
The carnitine derivatives of fatty acids are utilized for
A. One of the intermediates during b oxidation
B. Transporting fatty acids across the plasma membrane of the cell
C. Carrying fatty acids during fatty acid synthesis
D. Transporting fatty acids in plasma
E. Shuttling fatty acids across the mitochondrial membrane
E. Shuttling fatty acids across the mitochondrial membrane
Glycolysis and the TCA cycle are regulated by the cellular concentration of ATP, citrate and NADH, which provide a synchronized regulation of these two pathways through their committing enzymes. These enzymes are
A. Hexose kinase and alpha-ketoglutarate dehydrogenase
B. Phosphofructokinase-1 and isocitrate dehydrogenase
C. Glucokinase and isocitrate dehydrogenase
D. Pyruvate kinase and Succinyl CoA dehydrogenase
E. Phosphofructokinase-1 and Citrate dehydrogenase
B. Phosphofructokinase-1 and isocitrate dehydrogenase
Which of the following compounds is a potent stimulator of palmitate synthesis, an allosteric activator of acetyl-CoA carboxylase, and a source of both cytoplasmic acetyl-CoA and NADPH for lipogenesis?
A. Pantothenic acid
B. Glucose 6-phosphate
C. L-carnitine
D. Citrate
E. Biotin
D. citrate
Triacylglycerol molecules stored in adipose tissue represent the major reserve of substrate providing energy during a prolonged fast. During such a fast
A. The stored fatty acids are released from adipose tissue into the plasma as components of the serum lipoprotein particle, VLDL.
B. Hormone sensitive lipase is phosphorylated and activated by cAMP activated protein kinase
C. Glycerol produced by the degradation of triacylglycerol is an important direct source of energy for adipocytes and fibroblases
D. Free fatty acids are produced at a high rate in the plasma by the action of lipoprotein lipase on chylomicrons
E. Hormone-sensitive lipase is dephosphorylated and deactivated by protein phosphatase 1.
B. Hormone sensitive lipase is phosphorylated and activated by cAMP activated protein kinase
Which of the following is responsible for the down regulation of fatty acid synthesis under LOW energy conditions
A. Release of ATP inhibition of acetyl CoA carboxylase
B. AMP activation of AMPK
C. AMP activation of PFK-1
D. Release of ATP inhibition of carnitine acyltransferase 1
E. AMP activation of PEP carboxykinase
B. AMP activation of AMPK
When fatty acid biosynthesis is stimulated, beta oxidation of fatty acids is inhibited. This inhibition occurs mainly because:*
A. High levels of ATP inhibit AMPK, which prevents acetyl CoA carboxylase 1 from being phosphorylated, keeping synthesis "on"
B. Acetyl-CoA activates pyruvate carboxylase
C. High levels of ATP inhibit phosphofructokinase
D. Malonyl-CoA inhibits carnitine acyltransferase I
E. The pool of acetyl-CoA is depleted by the TCA cycle and fatty acid biosynthesis
D. Malonyl-CoA inhibits carnitine acyltransferase I
Fatty acid synthesis requires the presence of acetyl CoA. Does acetyl CoA affect the process of gluconeogenesis?
A. No, lipid metabolism and carbohydrate metabolism make use of completely different pathways and there are no direct connections between the two. Carbohydrates are formed from three carbon precursors and lipids from two carbon sources
B. No, one thing for certain is that fatty acids (and acetyl CoA made from these fatty acids) cannot be used to synthesize glucose
C. No, Acetyl CoA is formed in the mitochondria either by the action of pyruvate dehydrogenase or the enzymes of fatty acid oxidation. Gluconeogenesis takes place in the cytosol so that the metabolic pathways are seperated
D. Yes, Burning fatty acids provides both the ATP and the carbon skeletons needed to form glucose. Therefore the presence of acetyl CoA informs the cell that both energy and carbon are available for gluconeogenesis
E. Yes, The presence of acetyl CoA signals the cell that there is an excess of energy. While the acetyl CoA itself cannot be used to form glucose, its presence can activate pyruvate carboxylase which is needed to start gluconeogenesis.
E. Yes, The presence of acetyl CoA signals the cell that there is an excess of energy. While the acetyl CoA itself cannot be used to form glucose, its presence can activate pyruvate carboxylase which is needed to start gluconeogenesis.
The TCA cycle feeds into the biosynthesis of various products. Which of the following is not true?
A. Citrate feeds into fatty acid and sterol synthesis
B. Alpha ketoglutarate feeds into purine synthesis
C. Oxaloacetate feeds into glucose synthesis
D. Succinyl CoA feeds into Heme biosynthesis
E. Malate feeds into amino acid synthesis
E. Malate feeds into amino acid synthesis
Which liver enzyme is active in BOTH the fed and active state?
A. Pyruvate carboxylase
B. Pyruvate dehydrogenase
C. PFK2
D. Acetyl CoA carboxylase
E. Carnitine palmitoyltransferase 1
A. Pyruvate carboxylase
During Diabetic Ketosis when insulin is absent, fats are released and processed by beta oxidation. Which of the following are true?
i. Acetyl CoA reacts with oxaloacetate to create alpha-ketoglutarate and processed by TCA cycle
ii. In the absence of insulin there is a depletion of oxaloacetate and accumulation of Acetyl CoA
iii. Acetyl CoA can feed into the formation of ketone bodies and excess ketone body production can lower blood pH in diabetics
A. i. and ii.
B. ii. and iii
C. i. and iii
D. All of the above
E. None of the above
B. ii. and iii
Which of the following is NOT true about fatty acid synthesis?
A. The coenzyme for the oxidation and reduction reactions is NADP+/NADPH
B. Intermediates are linked to acyl carrier proteins.
C. The coenzyme for oxidation and reduction reactions is NADP+/NADPH
D. Fatty Acid synthesis occurs in the mitochondria
E. Intermediates are linked to acyl carrier proteins
D. Fatty Acid synthesis occurs in the mitochondria
What is the role of biotin in the beta-oxidation of ODD chain fatty acids
A. Biotin adds CoA to odd carbon acyl chains
B. Biotin removes phosphate from ATP to form carboxyphosphate
C. Biotin takes part in the addition of a CO2 from propionyl CoA
D. Biotin removes the terminal carbon to make and even numbered chain
E. Biotin removes CO2 from the odd carbon chain
C. Biotin takes part in the addition of a CO2 from propionyl CoA
Humans cannot achieve NET glucose synthesis from even carbon fatty acids due to the inability to convert:
A. acetyl CoA to malonyl CoA
B. Acetyl CoA to acetoacetate
C. Acetyl CoA to Pyruvate
D. Methylmalonyl CoA to succinyl CoA
E. Oxaloacetate to pyruvate
C. Acetyl CoA to Pyruvate
Beta-oxidation of fatty acids with even numbers of carbons will produce all of the following except
A. Butyryl CoA
B. NADH
C. FADH2
D. Malonyl CoA
E. Acetyl CoA
A. Butyryl CoA
The end product of glycolysis is pyruvate. However, pyruvate cannot directly enter TCA cycle. What needs to happen to pyruvate for the TCA cycle to proceed
A. Pyruvate must lose a CO2 when it reacts with TPP and form hydroxyethyl-TPP
B. Acetyl group linked to TPP must be transferred to lipoamide
C. Pyruvate must lose a CO2 when it reacts with TPP and form hydroxyethyl-TPP. CoA-SH acquires an acetyl group to make acetyl CoA
D. CoA-SH acquires an acetyl group to make acetyl CoA
E. Pyruvate must lose a CO2 when it reacts with TPP and form hydroxyethyl-TPP. Acetyl group linked to TPP must be transferred to lipoamide
E. Pyruvate must lose a CO2 when it reacts with TPP and form hydroxyethyl-TPP. Acetyl group linked to TPP must be transferred to lipoamide
The fate of acetate, the product of ethanol metabolism is which of the following?
A. Toxic to the tissues of the body and can lead to hepatic necrosis
B. Enters the TCA cycle directly to be oxidized
C. Is excreted in bile
D. Is taken up by other tissues and activated to acetyl CoA
E. Converted to NADH by ADH enzyme
D. Is taken up by other tissues and activated to acetyl CoA
Which of the following would be expected to occur after alcohol ingestion
A. Activation of fatty acid oxidation
B. Increase in gluconeogenesis
C. Inhibition of ketogenesis
D. Decrease in NAD+/NADH ratio
E. Lactic Acidosis
E. Lactic acidosis
The synthesis of glucose from pyruvate by gluconeogenesis:
A. requires the participation of biotin.
B. Occurs exclusively in the cytosol.
C. Requires the oxidation/reduction of FAD.
D. Involves lactate as an intermediate.
E. t Is inhibited by an elevated level of glucagon.
A. requires the participation of biotin.
Which one of the following is a common intermediate in the conversion of glycerol and lactate to glucose?
A. Malate
B. Phosphoenol pyruvate
C. Oxaloacetate
D. Pyruvate
E. Glucose 6-phosphate
E. Glucose 6-phosphate
Which one of the following reactions is unique to gluconeogenesis?
A. Glucose-6-PO4 to Fructose-6-PO4
B. Phosphoenolpyruvate to pyruvate
C. Lactate to pyruvate
D. 1,3-Bis-phosphoglycerate to 3-phosphoglycerate
E. Oxaloacetate to phosphoenolpyruvate
E. Oxaloacetate to phosphoenolpyruvate
Which of the following would be expected to occur after acute alcohol ingestion?
A. Lactic acidosis
B. An increase in NAD/NADH+ ratio
C. The activation of fatty acid oxidation
D. The inhibition of ketogenesis
E. An increase in gluconeogenesis
A. Lactic acidosis
A 34-year-old woman presents to her physician complaining of oral ulcers. A careful history reveals that she is a strict vegetarian and does not eat meat, fish, poultry, eggs, or dairy products. She is found to have a severe riboflavin deficiency. The function of which enzymes in the TCA cycle would be most directly affected by the riboflavin deficiency?
A. Aconitase
B. Malate dehydrogenase
C. Citrate synthase
D. Succinate dehydrogenase
E. Isocitrate dehydrogenase
D. Succinate dehydrogenase
Mammalian pyruvate dehydrogenase complex (PDC) is inactivated by pyruvate dehydrogenase kinase in the presence of:
A. Low Glucagon
B. High ADP
C. High Pyruvate
D. High NADH
E. High AMP
D. High NADH
Which lipoprotein particle functions in "reverse" cholesterol transport?
A. IDL
B. HDL
C. Chylomicrons
D. LDL
E. VLDL
B. HDL
Which of these enzymes is primarily responsible for digesting dietary triacylglycerols in the small intestine?
A. Pancreatic lipase
B. Lipoprotein lipase
C. Lingual lipase
D. Hormone-sensitive lipase
E. Gastric lipase
A. Pancreatic lipase
Which of the following would be associated with HIGH pyruvate dehydrogenase rate?
A. Low ATP
B. High Acetyl CoA
C. High ATP
D. Low acetyl-CoA
E. Low NAD+
F. Low pyruvate
G. LowNADH
A.Low ATP.
D. Low acetyl-CoA
G.Low NADH
The hallmarks of acute alcoholism without food intake are acidosis and hypoglycemia. These metabolic changes are due to the:
A. Metabolism of ethanol, which prevents the production of sufficient levels of blood glucose from lactate, glycerol and alanine.
B. Metabolism of ethanol, which prevents the production of sufficient levels of blood glucose from glycogen stores.
C. Lack of food uptake (glucose) and the cellular metabolism of alcohol generates high concentration of NADPH, which is favorable for ketoacids production.
D. Oxidation of alcohol in the liver produces large amounts of acetyl-CoA that increases the ketone bodies production and reduces gluconeogenesis.
E. An increase in the use of the glycolytic pathway. The use of glycolysis rather than the electron transport chain to produce ATP would result in a deficiency of energy in the liver cell.
A. Metabolism of ethanol, which prevents the production of sufficient levels of blood glucose from lactate, glycerol and alanine.
Hormonal activation of cyclic AMP levels will:
A. Phosphorylate PFK2 on a tyrosine residue.
B. Activate the PKC phosphorylation of PFK2.
C. Increase the activation of gluconeogenesis.
D. activate protein kinase A phosphorylation of Fructose bisphosphatase 2.
E. Lead to the activation of PFK.
C. Increase the activation of gluconeogenesis.
Which of the following vitamins are precursors to coenzymes that are necessary for the formation of acetyl CoA from pyruvate?
A. Thiamine, riboflavin, and lipoic acid
B. Thiamine, riboflavin, niacin, and biotin
C. Thiamine, riboflavin, niacin, lipoic acid, and pantothenic acid
D. Thiamine, riboflavin, niacin, lipoic acid, pantothenic acid, and biotin
C. Thiamine, riboflavin, niacin, lipoic acid, and pantothenic acid
In addition to pyruvate dehydrogenase, what other enzyme(s) in the citric acid cycle has a key thiamine pyrophosphate coenzyme?
A. Citrate synthase
B. Isocitrate dehydrogenase
C. α-ketoglutarate dehydrogenase
D. Aconitase
E. Malate dehydrogenase
C. α-ketoglutarate dehydrogenase
Why does acetyl CoA, a product of fatty acid catabolism, influence the pyruvate dehydrogenase complex (PDH), a control point in carbohydrate catabolism?
A. When fatty acid breakdown is inhibited, ADP is low, causing a decrease in activity.
B. When fatty acid breakdown is high, PDH is inhibited by acetyl CoA due to pyruvate kinase activity.
C. When fatty acid breakdown is high, NADH levels drop, causing an increase in E2 activity.
D. When fatty acid breakdown is high, ADP is low and PDH is inhibited by phosphatase activity.
E. When fatty acid breakdown is inhibited, PDH is inhibited by acetyl CoA due to phosphatase activity.
B. When fatty acid breakdown is high, PDH is inhibited by acetyl CoA due to pyruvate kinase activity.
The citric acid cycle is activated in the presence of oxygen (O2), but what is the link between the citric acid cycle and O2?
A. The iron-sulfur center requires O2 to be in the appropriate oxidation state.
B. The one substrate-level phosphorylation in the citric acid cycle can occur in the absence of O2.
C. O2 is an allosteric activator for citrate synthase.
D. A primary product of the citric acid cycle is NADH, the principle electron donor to the O2, the last electron acceptor in the electron-transport system.
E. The presence of O2 in the mitochondrial matrix releases CO2 into the cytosol.
D. A primary product of the citric acid cycle is NADH, the principle electron donor to the O2, the last electron acceptor in the electron-transport system.
What is(are) the chemical change(s) involved in the conversion of citrate into isocitrate?
A. Oxidation
B. Oxidative decarboxylation
C. Dehydration followed by hydration
D. Oxidation followed by reduction
E. Hydration followed by dehydration
C. Dehydration followed by hydration
Which of the following conditions will activate pyruvate dehydrogenase kinase, which catalyzes the phosphorylation and inactivation of E1 in the pyruvate dehydrogenase complex?
A. Ca2+
B. Elevated concentrations of acetyl CoA
C. Elevated concentrations of NADH and ATP
D. Elevated c
C. Elevated concentrations of NADH and ATP
The direct movement of substrates from one enzyme to the next is called:
A. Cell with sufficient available water.
B. Substrate channeling.
C. Protein complex.
D. Electron acceptor.
E. Linker coenzyme.
B. Substrate channeling.
A mutation in the active site of succinyl CoA synthetase where His is converted to Lys would result in which of the following?
A. Increased stable folding
B. Loss of a positively charged amino acid necessary for catalysis
C. Loss of a succinyl phosphate intermediate
D. All of the above
E. None of the above
C. Loss of a succinyl phosphate intermediate
What are the steps involved (in order) in the conversion of pyruvate to acetyl CoA?
A. Oxidation, decarboxylation, transfer to CoA
B. Decarboxylation, transfer to CoA, oxidation
C. Decarboxylation, oxidation, transfer to CoA
D. Oxidation, transfer to CoA, decarboxylation
E. Oxidation, dehydration, transfer to CoA
C. Decarboxylation, oxidation, transfer to CoA
Approximately how many ATP or GTP equivalents are produced during one turn of the citric acid cycle?
A. 32
B. 10
C. 6
D. 9
E. 12
B. 10
Although we study the citric acid cycle as the final stage oxidation of carbon from glucose, an in-depth look at the cycle shows intermediates entering and leaving the cycle from a number of metabolic pathways. With all of these demands on the cycle, how does it maintain a minimal level of oxaloacetate (OAA) to allow the cycle to function?
A. Isocitrate dehydrogenase is allosterically inhibited by ADP, which signifies the need for more energy.
B. OAA is synthesized via pyruvate carboxylase in an anaplerotic reaction that occurs when acetyl CoA is present.
C. OAA is formed directly via the deamination of glutamate.
D. The rate of the cycle is increased when the cell has high levels of NADH.
E. OAA can be formed by the condensation of two moles of acetyl CoA and occurs when the energy charge of the cell is high
B. OAA is synthesized via pyruvate carboxylase in an anaplerotic reaction that occurs when acetyl CoA is present.
A 1-month-old male showed abnormalities of the nervous system and lactic acidosis. Enzyme assay for pyruvate dehydrogenase (PDH) activity on extracts of cultured skin fibroblasts showed 5% of normal activity, with a low concentration (1 x 10-4 mM) of thiamine pyrophosphate (TPP), but 80% of normal activity when the assay contained a high (0.4 mM) concentration of TPP. Which one of the following statements concerning this patient is most correct?
A. Administration of thiamine is expected to reduce his serum lactate concentration and improve his clinical symptoms.
B. A diet consisting of high carbohydrate intake would be expected to be beneficial in this patient.
C. Alanine concentration in the blood is expected to be less than normal.
D. The patient is expected to show disturbances in fatty acid degradation.
E. Elevated levels of lactate and pyruvate in the blood reliably predict the presence of PDH deficiency.
A. Administration of thiamine is expected to reduce his serum lactate concentration and improve his clinical symptoms.
A low level of carbon dioxide labeled with 14C is accidentally released into the atmosphere surrounding industrial workers as they resume work following the lunch hour. Unknowingly, they breathe the contaminated air for 1 hour. Which of the following compounds will be radioactively labeled?
A. About one third of the carbons of newly synthesized malonyl CoA
B. About one half of the carbon atoms of newly synthesized fatty acids.
C. The carboxyl atom of newly synthesized fatty acids.
D. All of the carbon atoms of newly synthesized fatty acid.
E. One half of the carbon atoms of newly synthesized acetyl CoA.
A. About one third of the carbons of newly synthesized malonyl CoA
Fatty acid synthesis is regulated by hormone depending on feeding vs. fasting and recent exercise vs. no recent exercise. Which hormones are active and what is their mechanism of action of the(se) hormone(s) after exercise and a meal?
A. Epinephrine stimulates the mobilization of fatty acids and stimulates their accumulation as triacylglycerols.
B. Insulin stimulates the mobilization of fatty acids for β oxidation.
C. Epinephrine stimulates AMPK, preventing the phosphorylation of acetyl CoA carboxylase 1.
D. Insulin stimulates fatty acid synthesis by activating acetyl CoA carboxylase 1.
E. Glucagon activates the carboxylase by enhancing the phosphorylation of AMPK.
D. Insulin stimulates fatty acid synthesis by activating acetyl CoA carboxylase 1.
What are the conditions that lead to a "beer gut" due to the excess consumption of alcohol?
A. The processing of acetate in the liver becomes inefficient leading to a pH imbalance in liver cells, reducing enzyme efficiency in general.
B. NADH produced from the metabolism of ethanol stimulates the citric acid cycle for glucose-derived acetyl CoA.
C. NADH inhibits ketone body formation, stimulating glucose rather than fatty acid metabolism.
D. NADH stimulates citric acid cycle enzymes that stimulates glucose-derived acetyl CoA metabolism.
E. Excess ethanol metabolism leads to an accumulation of NADH that inhibits fatty acid metabolism.
E. Excess ethanol metabolism leads to an accumulation of NADH that inhibits fatty acid metabolism.
A 20-year-old woman with diabetes mellitus was admitted to the hospital in a semi-conscious condition with fever, nausea and vomiting. The woman's breath smelled of acetone. A urine sample was strongly positive for ketone bodies. In this patient:
A. The patient should be given an intravenous infusion of glucose to regain consciousness.
B. The acetone must have been produced by spontaneous decarboxylation of β-hydroxybutyrate.
C. A blood glucose test would likely show that her blood glucose was well below 80 mg/dL.
D. An insulin injection would alleviate her ketoacidosis by decreasing ketone body production.
E. Glucagon should be administered immediately to stimulate glycogenolysis and gluconeogenesis in the liver.
D. An insulin injection would alleviate her ketoacidosis by decreasing ketone body production.
Increased expression of the enzyme cytochrome P450 2E1 in chronic alcoholics would result in which of the following?
A. an increased clearance of ethanol from the blood.
B. Protection from liver damage.
C. A decreased clearance of ethanol from the blood.
D. A decrease in the rate of acetaldehyde production.
E. A decrease of one's alcohol tolerance level.
A. an increased clearance of ethanol from the blood.
A person has entered a hunger strike. After five days of starvation, what kind of fuel is being utilized?
A. Glycogen stored in the liver
B. Glycogen and protein from the liver
C. Glycogen stored in the muscle
D. Protein from skeletal muscle and fat from adipose tissue
E. Protein from the brain and heart
D. Protein from skeletal muscle and fat from adipose tissue