Other Lipid Catabolism Concepts
Practice Questions
Biochemistry › Other Lipid Catabolism Concepts
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.
Which is not a chemical reaction fundamental to peroxisomes?
Which of the following characterizes the differences between chloroplasts and mitochondria as regards the way their relationship to lipids?
Cholesterol and triglycerides are transported in the blood by lipoproteins. These lipoproteins are: very low density proteins (VLDL), high density proteins (HDL), intermediate density proteins (IDL), chylomicrons and low-density proteins (LDL). Which of the following is true regarding these lipoproteins?
Long-chain fatty acids are broken down through beta-oxidation in the mitochondrial matrix. The result is an abundance of acetyl-CoA which can then go onto the Krebs cycle and oxidative phosphorylation. However, when plasma glucose is low, stores of oxaloacetate are depleted to form more glucose, and the Krebs cycle becomes unable to incorporate all of the acetyl-CoA from beta-oxidation.
What is the fate of the resultant excess of acetyl-CoA?
A deficiency of an enzyme in lipid metabolism leads to high levels of triglycerides in the blood. What is the name of the deficient enzyme most likely involved?
How do high-density lipoproteins (HDL) remove cholesterol from the periphery?
I. HDL transfer cholesterol to liver cells through the scavenger receptor SR-B1
II. HDL transfer cholesterol to intermediate-density lipoproteins using the cholesterol transfer protein
III. HDL removes cholesterol accumulating in blood vessels
IV. HDL is taken up by macrophages in atherosclerotic plaques
What happens when the acetyl-CoA produced from beta-oxidation can not enter into the Krebs Cycle due to a lack of oxaloacetate from starvation?
After beta oxidation of a fatty acid with an odd number of carbons in its carbon chain, propionyl-CoA is produced. How does this molecule enter into the Krebs cycle?
Where in a cell are fatty acids broken down via 