Cholesterol Metabolism and Vascular Disease

Cholesterol is packaged into lipoprotein particles in the liver and intestine and transported to peripheral tissues for normal cellular function. Reverse cholesterol transport is the mechanism by which excess cholesterol is transported back to the liver and is facilitated by high-density lipoproteins (HDLs). Increased plasma concentrations of cholesterol within the low-density lipoprotein (LDL) contribute to atherosclerotic vascular disease that commonly affects the coronary, cerebral and peripheral vascular circulation. Incontrovertible evidence now supports the use of the ‘statin’ class of drugs to decrease vascular disease. Statins inhibit hepatic cholesterol synthesis, increase hepatic low-density lipoprotein cholestrol (LDLc) receptor expression and consequently decrease plasma LDLc, to reduce risk of myocardial infarction in people at widely varying risk of heart disease. At present, there is limited evidence to support the use of drugs that modify high-density lipoprotein cholesterol (HDLc) to reduce risk of heart disease.

Key concepts

  • Endogenous and exogenous lipid pathways.
  • Hypercholesterolaemias.
  • Low-density lipoprotein cholesterol (LDLc) and heart disease.
  • High-density lipoprotein (HDL) metabolism.
  • Modification of high-density lipoprotein cholesterol (HDLc) and heart disease.
  • Pathophysiology of vascular disease in relation to lipid metabolism.

Keywords: cholesterol; atherosclerotic vascular disease; randomized trials

Figure 1. Relationship between dietary nutrients, lipid synthesis, lipoproteins and atherosclerotic vascular disease. HMGCoA, hydroxymethylglutaryl coenzyme A.
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Olufadi, R, Wild, SH, and Byrne, CD(Sep 2009) Cholesterol Metabolism and Vascular Disease. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0002264.pub2]