Cholesterol Metabolism and Biosynthesis Flashcards

Flashcards on Cholesterol Metabolism and Biosynthesis

Cholesterol

Has a crucial role as a component of cell membranes and as a precursor of steroid hormones and bile acids.

Atherosclerosis

A disease caused by cholesterol build-up in blood vessels that results in obstruction of blood vessels.

Acetate

A single simple precursor that supplies all carbons in the biosynthesis of cholesterol.

Isoprene

An intermediate involved in cholesterol biosynthesis, also a precursor to many other lipids.

HMG-CoA Reductase

An enzyme that reduces HMG-CoA to form Mevalonate during cholesterol biosynthesis.

Squalene

A non-cyclic intermediate formed during cholesterol biosynthesis, through the head to head condensation of two farnesyl pyrophosphates.

Lanosterol

An intermediate formed through cyclisation in animals and is converted to cholesterol through a series of 20 reactions.

Biliary Cholesterol

One form in which cholesterol is exported from the liver into the intestines.

Bile Acids

One form in which cholesterol is exported from the liver into the intestines, aiding in lipid digestion.

Cholesteryl Esters

One form in which cholesterol is exported from the liver into the bloodstream for transport, an even more hydrophobic form of cholesterol.

ACAT (Acyl-CoA-cholesterol acyl transferase)

An enzyme expressed in a range of tissues (e.g. liver/skin) that is activated by high cholesterol to makes cholesteryl esters.

Plasma Lipoproteins

Substances that transport cholesterol and differ in composition, ranging in density from chylomicrons to HDLs, examples including LDL.

Apolipoproteins

Dictate the function of plasma lipoproteins.

LDL receptor

Receptor involved in cholesterol import into the liver and other tissues.

ABC Transporters

Move cholesterol across cell membranes (in extrahepatic tissues) towards HDL particles.

LCAT

Esterifies cholesterol on HDL particles.

SREBPs (Sterol regulatory element-binding proteins)

Bind to SREBP cleavage activating protein (SCAP) and are inactive when cholesterol levels are high.

Hormonal Control

Covalent modification of HMG-CoA reductase by phosphorylation, glucagon stimulates phosphorylation (INACTIVE), insulin stimulates dephosphorylation (ACTIVE).

Familial Hypercholesterolemia

Individuals have defective LDL receptor, resulting in very high levels of cholesterol due to inefficient clearing from the blood.

Statins

Competitive inhibitors of HMG-CoA reductase that mimic mevalonate.