Cholesterol and Lipid Digestion, Absorption, and Transport

A set of 23 vocabulary flashcards summarizing essential terms related to cholesterol and lipid digestion, absorption, and transport.

Cholesterol

Contains a rigid ring structure with 4 fused rings, a polar head group (HO), and a hydrophobic hydrocarbon tail

Steroid nucleus

The common four fused-ring (A–D) core structure found in cholesterol, steroid hormones (cortisol, testosterone, etc.), and several fat-soluble vitamins (Vit D, E, K1/K2, A).

Chylomicron

A very large, low density, triglyceride-rich (fat-rich) lipoprotein assembled from emulsification droplets in the intestines.

Lipoprotein

A spherical complex of triglycerides, proteins, free cholesterol, cholesterol-bound fatty acids, and a phospholipid bilayer

High-Density Lipoprotein (HDL)

The smallest, protein-rich lipoprotein that scavenges excess cholesterol from tissues and returns it to the liver (reverse cholesterol transport). Contains ApoA-I and II, Apo E, and Apo C

Low-Density Lipoprotein (LDL)

A cholesterol-rich lipoprotein derived from VLDL/IDL that delivers cholesterol to tissues. Any unused particles are recycled to the liver (good) or scavanged by macrophages, which contributes to atherosclerosis (bad).

Very-Low-Density Lipoprotein (VLDL)

A triglyceride-rich lipoprotein secreted by the liver to export endogenous fat; becomes IDL and LDL after lipolysis.

Intermediate-Density Lipoprotein (IDL)

A transitional lipoprotein with approximately equal proportions of fats, cholesterol, and protein.

Apolipoprotein B-48 (ApoB-48)

Only on chylomicrons, binds particles to cells

Apolipoprotein B-100 (ApoB-100)

The main structural protein of VLDL, IDL, and LDL. Binds particles to cells

Apolipoprotein C-II (ApoC-II)

Found on chylomicron, VLDL, IDL, HDL; activates LDL to free FAs from triglycerides

Apolipoprotein E (ApoE)

An apoprotein on chylomicron, VLDL, IDL, and HDL; assists in binding of particles to cells

Bile Salts/Acids

Contains four-ring structure with two R groups (R1 = OH or H; R2 = OH, NH-CH2-COOH, or NH-CH2-CH2-SO3H); assists in emulsification of fat globules.

Emulsification

The dispersion of large fat globules into tiny micelles by bile salts, increasing surface area for pancreatic lipase action.

Receptor-Mediated Endocytosis of LDL

1. LDL receptor synthesized in rough ER → LDL receptor to plasma membrane via Golgi

2. LDL receptor binds ApoB-100 on LDL, initiating endocytosis

3. LDL internalized in endosome; LDL receptor is segregated into a vesicle and recycled to cell surface, while endosome with LDL fuses with lysosome

4. Lytic enzymes in lysosome degrade ApoB-100 and cholesterol esters, releasing AAs, triacylglycerol, and cholesterol

Foam Cell

A macrophage engorged with cholesterol and lipids. Formed by eating LDL. Foam cells become lodged in artery as plaque, so blood path is narrowed. These plaques can rupture (atherosclerosis), or the fibrous caps that form can rupture because they are unstable.

Phase Transition Temperature (Tm)

The temperature at which a membrane shifts from an ordered to a fluid state. Stronger molecular forces increase Tm (longer, saturated chains). Cholesterol helps to resist the transition phase, creating a linear transition rather than a sharp collapse

Reverse Cholesterol Transport: Path of HDL

HDL created in liver, and sent through bloodstream. HDL gives ApoE and ApoCII to VLDL, and takes them back from IDL. HDL then picks up excess cholesterol from LDL for delivery back to liver

Chylomicron Pathway

1. bile salts emulsify dietary fats in s. intestine, forming mixed micelles; intestinal lipases degrade triglycerides into FFAs

2. FAs are taken up by intestinal mucosa and converted into triglycerides; chylomicrons are formed

3. Chylomicrons move into the lymph, then the bloodstream

4. Lipoprotein lipase (LPL) is activated by ApoCII, releasing FFA, which can be oxidized as fuel or put into storage. Chylomicron remnants travel to the liver for disassembly.

Lipoprotein pathway

1. VLDL created in the liver (has ApoB100). VLDL travels through the bloodstream, maturing into mature VLDL, which is rich in TG and contains ApoB100, ApoE, and ApoCII

2. LPL converts VLDL into IDL (which has fewer TG), other TG is taken up by other tissues

3. IDL loses ApoCII and ApoE, forming LDL, which is rich in cholesterol

4. Particles (with cholesterol) are taken up by tissues, and LDL particles not taken up are returned to the liver or scavenged by macrophages