Lipid Catabolism
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Biochemistry › Lipid Catabolism
Which reaction in beta oxidation does hydroxyacyl-CoA dehydrogenase catalyze?
Oxidation of the beta hydroxyl group
Reduction of the beta hydroxyl group
Oxidation the gamma carbon
Dehydration of the beta carbon
Dehydration of the carbonyl carbon
Explanation
Hydroxyacyl-CoA dehydrogenase oxidizes the beta hydroxyl group, forming a carbonyl.

Why does consuming alcohol (ethanol) promote storage of fatty acids in the form of triglycerides (fatty tissue), especially in the liver?
The produced from ethanol oxidation to acetaldehyde inhibits fatty acid oxidation, causing them to be stored as triglycerides
The produced from ethanol oxidation to acetaldehyde inhibits fatty acid oxidation, causing them to be stored as triglycerides
The acetaldehyde produced from ethanol directly inhibits enzymes which oxidize fatty acids
The free radicals produced in this process directly inhibit enzymes which oxidize fatty acids
Ethanol directly inhibits the enzymes which oxidize fatty acids by binding to their active sites
Explanation
The oxidation of ethanol to acetaldehyde in the liver produces , leading to an elevated
ratio. Multiple enzymes responsible for fatty acid oxidation are under control of this ratio; they are active when there is more
an inactive when there is more
. Thus, they become inactivated, and fatty acids are stored in the liver as triglycerides - this is why alcoholism leads to fatty liver disease. Free radicals can damage the liver and other tissues but do not directly inhibit these enzymes; neither does the ethanol molecule itself nor acetaldehyde
Which reaction in beta oxidation does hydroxyacyl-CoA dehydrogenase catalyze?
Oxidation of the beta hydroxyl group
Reduction of the beta hydroxyl group
Oxidation the gamma carbon
Dehydration of the beta carbon
Dehydration of the carbonyl carbon
Explanation
Hydroxyacyl-CoA dehydrogenase oxidizes the beta hydroxyl group, forming a carbonyl.

Why does consuming alcohol (ethanol) promote storage of fatty acids in the form of triglycerides (fatty tissue), especially in the liver?
The produced from ethanol oxidation to acetaldehyde inhibits fatty acid oxidation, causing them to be stored as triglycerides
The produced from ethanol oxidation to acetaldehyde inhibits fatty acid oxidation, causing them to be stored as triglycerides
The acetaldehyde produced from ethanol directly inhibits enzymes which oxidize fatty acids
The free radicals produced in this process directly inhibit enzymes which oxidize fatty acids
Ethanol directly inhibits the enzymes which oxidize fatty acids by binding to their active sites
Explanation
The oxidation of ethanol to acetaldehyde in the liver produces , leading to an elevated
ratio. Multiple enzymes responsible for fatty acid oxidation are under control of this ratio; they are active when there is more
an inactive when there is more
. Thus, they become inactivated, and fatty acids are stored in the liver as triglycerides - this is why alcoholism leads to fatty liver disease. Free radicals can damage the liver and other tissues but do not directly inhibit these enzymes; neither does the ethanol molecule itself nor acetaldehyde
Before a fatty acid is able to undergo the beta-oxidation pathway, it must first be activated to form fatty acyl-CoA and transferred into the mitochondrial matrix from the cytoplasm of a cell via the activity of several enzymes.
What enzyme is responsible for synthesizing fatty acyl-CoA to be transported into the intermembrane space of a mitochondria?
acyl-CoA synthetase
Carnitine palmitoyl transferase I
Carnitine palmitoyl transferase II
ATP hydrolase
Citrate synthase
Explanation
Three enzymes are ultimately involved in activating fatty acids as fatty acyl-CoA and transferring this molecule into the inner mitochondrial matrix to be broken down via the beta-oxidation pathway. The first enzyme is acyl-CoA synthetase. This enzyme is a type of ATPase, and it uses the thermodynamically favorable dephosphorylation of ATP to drive the synthesis of fatty acyl-CoA from a fatty acid and CoASH. Fatty acids alone cannot cross mitochondrial membranes, but fatty acyl-CoA can cross the outer membrane.
Carnitine palmitoyl transferase II also synthesizes fatty acyl-CoA but acyl-CoA synthetase is the first enzyme to do so, and its dephosphorylation of ATP is what initially activates a fatty acid.
Before a fatty acid is able to undergo the beta-oxidation pathway, it must first be activated to form fatty acyl-CoA and transferred into the mitochondrial matrix from the cytoplasm of a cell via the activity of several enzymes.
What enzyme is responsible for synthesizing fatty acyl-CoA to be transported into the intermembrane space of a mitochondria?
acyl-CoA synthetase
Carnitine palmitoyl transferase I
Carnitine palmitoyl transferase II
ATP hydrolase
Citrate synthase
Explanation
Three enzymes are ultimately involved in activating fatty acids as fatty acyl-CoA and transferring this molecule into the inner mitochondrial matrix to be broken down via the beta-oxidation pathway. The first enzyme is acyl-CoA synthetase. This enzyme is a type of ATPase, and it uses the thermodynamically favorable dephosphorylation of ATP to drive the synthesis of fatty acyl-CoA from a fatty acid and CoASH. Fatty acids alone cannot cross mitochondrial membranes, but fatty acyl-CoA can cross the outer membrane.
Carnitine palmitoyl transferase II also synthesizes fatty acyl-CoA but acyl-CoA synthetase is the first enzyme to do so, and its dephosphorylation of ATP is what initially activates a fatty acid.
Fatty acyl-CoA enters the intermembrane space of a mitochondria via the enzyme acyl-CoA synthetase. Fatty acyl-CoA is the original input molecule of the beta-oxidation pathway, however, carnitine palmitoyl transferase I replaces the CoA with the molecule carnitine before being transported into the mitochondrial matrix.
Why does carnitine palmitoyl transferase replace coenzyme A with carnitine?
The carnitine carrier protein can only attach and transport fatty acylcarnitine across the inner mitochondrial membrane.
Fatty acyl-CoA is to unstable of a molecule to exist within the intermembrane space.
The reformation of fatty acyl-CoA from CoASH and fatty acylcarnitine within the mitochondrial matrix is a thermodynamically favorable reaction that drives the formation of ATP.
Carnitine is needed as an input to start the beta-oxidation pathway.
Fatty acylcarnitine can freely diffuse into the mitochondrial matrix through fatty acylcarnitine gates located on the inner mitochondrial membrane.
Explanation
The carnitine transport protein, known as the carnitine-acylcarnitine translocase, allows the facilitated diffusion of a fatty acid into the mitochondrial matrix. Fatty acids cannot be transported into the mitochondrial matrix alone.
Following this step, carnitine palmitoyl transferase II catalyzes the reaction that reforms fatty acyl-CoA from CoASH and the fatty acylcarnitine.
Which of the following statements is true about the role of apolipoprotein B (ApoB)100 in lipid metabolism?
I. ApoB 100 is synthesized by the liver.
II. ApoB 100 is a component of very low density, intermediate density and low density lipoproteins circulating in the blood.
III. ApoB 100 is a ligand for the LDL (low density lipoprotein) receptor in cells requiring intake of cholesterol.
IV. ApoB 100 is encoded by the same gene that produces ApoB 48.
I, II, III, and IV
I, II, and III
II, III, and IV
I and II
I and IV
Explanation
Apoliporoteins carry lipids in the blood as lipids are insoluble. ApoB100 is a protein found on different types of lipoproteins circulating in the body. ApoB 48 is another apolipoprotein that is present on chylomicrons. Both ApoB 100 and ApoB 48 are encoded by the ApoB gene, but ApoB 48 is shorter than ApoB 100 and is produced in the intestine.
Which of the following statements is true about the role of apolipoprotein B (ApoB)100 in lipid metabolism?
I. ApoB 100 is synthesized by the liver.
II. ApoB 100 is a component of very low density, intermediate density and low density lipoproteins circulating in the blood.
III. ApoB 100 is a ligand for the LDL (low density lipoprotein) receptor in cells requiring intake of cholesterol.
IV. ApoB 100 is encoded by the same gene that produces ApoB 48.
I, II, III, and IV
I, II, and III
II, III, and IV
I and II
I and IV
Explanation
Apoliporoteins carry lipids in the blood as lipids are insoluble. ApoB100 is a protein found on different types of lipoproteins circulating in the body. ApoB 48 is another apolipoprotein that is present on chylomicrons. Both ApoB 100 and ApoB 48 are encoded by the ApoB gene, but ApoB 48 is shorter than ApoB 100 and is produced in the intestine.
Fatty acyl-CoA enters the intermembrane space of a mitochondria via the enzyme acyl-CoA synthetase. Fatty acyl-CoA is the original input molecule of the beta-oxidation pathway, however, carnitine palmitoyl transferase I replaces the CoA with the molecule carnitine before being transported into the mitochondrial matrix.
Why does carnitine palmitoyl transferase replace coenzyme A with carnitine?
The carnitine carrier protein can only attach and transport fatty acylcarnitine across the inner mitochondrial membrane.
Fatty acyl-CoA is to unstable of a molecule to exist within the intermembrane space.
The reformation of fatty acyl-CoA from CoASH and fatty acylcarnitine within the mitochondrial matrix is a thermodynamically favorable reaction that drives the formation of ATP.
Carnitine is needed as an input to start the beta-oxidation pathway.
Fatty acylcarnitine can freely diffuse into the mitochondrial matrix through fatty acylcarnitine gates located on the inner mitochondrial membrane.
Explanation
The carnitine transport protein, known as the carnitine-acylcarnitine translocase, allows the facilitated diffusion of a fatty acid into the mitochondrial matrix. Fatty acids cannot be transported into the mitochondrial matrix alone.
Following this step, carnitine palmitoyl transferase II catalyzes the reaction that reforms fatty acyl-CoA from CoASH and the fatty acylcarnitine.