Block 3 Lipoproteins Sem 1

1. Higher levels in the blood are correlated with a decreased risk of heart disease.

VLDL

Albumin

Chylomicrons

HDL

IDL

HDL is thought to exert a protective effect by acting as a transporter for cholesterol and cholesterol esters. Additionally, HDLs provide the apoproteins ncessary for VLDL and Chylomicron processing of TGs.

Explanation

HDL is thought to exert a protective effect by acting as a transporter for cholesterol and cholesterol esters. Additionally, HDLs provide the apoproteins ncessary for VLDL and Chylomicron processing of TGs.

2. Which statement below best describes the metabolic route of LDL ?

VLDL are acted on by lipoprotein lipase to form HDL which is converted to LDL.

VLDL are acted on by lipoprotein lipase to form IDL which is converted to LDL

It is made in the liver from chylomicron remnants

It is made in plasma from HDL.

Chylomicrons are acted on by lipoprotein lipase to form remnants which are converted to IDL and then LDL in plasma.

LDLs result from the maturation of VLDLs to IDLs and finally to LDLs

Explanation

LDLs result from the maturation of VLDLs to IDLs and finally to LDLs

3. What is the defect seen in patients with familial hypercholesterolemia (FHC)?

The LDL contains too much cholesterol to bind to the receptor.

The LDL contains a defective apo B100.

The lysosomes contain no cholesteryl esterase

The patient has no activator for the lipoprotein lipase

The patient has a defective receptor

A genetic defect; lack of functional receptor precludes proper processing, and LDL levels increase to pathologic levels

Explanation

A genetic defect; lack of functional receptor precludes proper processing, and LDL levels increase to pathologic levels

4. Activator of LCAT:

Apo C-II.

Apo B100.

Apo A-I.

Apo E

All of these.

Apo A-I is a key co-factor for LCAT.

Explanation

Apo A-I is a key co-factor for LCAT.

5. What is the rationale for trying to lower LDL by use of cholestyramine?

It is a competitive inhibitor of lipoprotein lipase

It decreases the number of class B type I Scavenger Receptors in fibroblasts

It down-regulates the synthesis of LDL receptors in liver.

It stimulates ACAT in cells and so depletes cellular free cholesterol.

It stimulates bile acid excretion in the feces.

Elimination of bile from the GI tract means that the liver must make more bile salts and will therefore need more cholesterol precursor, which can be recovered from the blood by increasing the number of liver LDL receptors.

Explanation

Elimination of bile from the GI tract means that the liver must make more bile salts and will therefore need more cholesterol precursor, which can be recovered from the blood by increasing the number of liver LDL receptors.

6. Which statement below about LDL is FALSE?

High levels indicate an increased risk of coronary artery disease

Its receptor binds to both apoB-100 and apoE

Its major apo protein is apoE.

On electrophoresis it migrates faster than chylomicrons.

The use of resins will upregulate LDL receptors on the surface of liver cells

Apo B100 is the major apoprotein found in LDLs

Explanation

Apo B100 is the major apoprotein found in LDLs

7. Which statement below about lipoprotein lipase is FALSE ?

It is absent in blood vessels found in adipose tissue.

It is attached to a glycosaminoglycan

It is responsible for hydrolysis of triglycerides

VLDL is one of its substrates

It requires apoprotein CII be present for activity

Lipoprotein lipase is attached to the capillary endothelium in adipose tissue, lactating breast tissue and skeletal muscle tissue.

Explanation

Lipoprotein lipase is attached to the capillary endothelium in adipose tissue, lactating breast tissue and skeletal muscle tissue.

8. Which statement below concerning LDL and oxidized LDL is TRUE?

Endothelial cells reduce oxidized LDL to native LDL.

Foam cells are formed during endothelial cell processing of LDL.

Oxidized LDL is chemotactic for monocytes

Free radicals containing oxygen prevent buildup of atherosclerotic plaques by destroying LDL.

NONE of the above is TRUE.

Excess LDL passes through the endothelial barrier and may be oxidized leading to a chemotactic attraction of monocytes (macrophages). The oxidized LDL undergoes phagocytosis by the macrophages thereby yielding a foam cell. Ultimately these cells undergo cell death and lysis leading to injury to the endothelial cells, with resultant metabolic processes that lead to atherosclerosis

Explanation

Excess LDL passes through the endothelial barrier and may be oxidized leading to a chemotactic attraction of monocytes (macrophages). The oxidized LDL undergoes phagocytosis by the macrophages thereby yielding a foam cell. Ultimately these cells undergo cell death and lysis leading to injury to the endothelial cells, with resultant metabolic processes that lead to atherosclerosis

9. Why is the rate of production of LDL increased in familial hypercholesterolemic (FHC) individuals?

Because IDL is removed more slowly from the circulation and so is converted into LDL.

Because VLDL synthesis is increased

Because IDL synthesis is increased

Because chylomicron synthesis is increased.

ALL of the above are correct

Decreased lipoprotein receptors or receptor occupancy leaves the IDLs in the blood stream where they are converted to LDLs. Remember that IDLs bind to those receptors that recognize ApoE including the LDL receptor. FHC individuals lack working LDL receptors.

Explanation

Decreased lipoprotein receptors or receptor occupancy leaves the IDLs in the blood stream where they are converted to LDLs. Remember that IDLs bind to those receptors that recognize ApoE including the LDL receptor. FHC individuals lack working LDL receptors.

10. Binds to a specfic cell receptor and is found on IDL but not on LDL.

Apo C-II

Apo B100

Apo B48

Apo E.

Apo A-I

Apo B and Apo E are found on IDL but Apo E is not on LDL.

Explanation

Apo B and Apo E are found on IDL but Apo E is not on LDL.

11. Which ONE of the following proteins allows HDL to off-load cholesterol esters?

Lipoprotein Lipase.

LCAT

ACAT

ApoAI

Scavenger Receptor Class B Type I.

An apoA-I mimetic peptide facilitates off-loading cholesterol from HDL to liver cells through scavenger receptor BI.

Excessive cellular cholesterol is transported to the liver by a pathway called 'reverse cholesterol transport.' Scavenger receptor class B, type I (SR-BI) mediates cholesterol uptake in the liver

LCAT functions in the plasma and forms CE in HDL by transferring polyunsaturated fatty acid from phosphatidylcholine to cholesterol.

Explanation

An apoA-I mimetic peptide facilitates off-loading cholesterol from HDL to liver cells through scavenger receptor BI.

Excessive cellular cholesterol is transported to the liver by a pathway called 'reverse cholesterol transport.' Scavenger receptor class B, type I (SR-BI) mediates cholesterol uptake in the liver

LCAT functions in the plasma and forms CE in HDL by transferring polyunsaturated fatty acid from phosphatidylcholine to cholesterol.