a1 Nutrition Department, Institut Pasteur de Lille, 1 rue du Professeur Calmette, BP 245, 59019 Lille Cedex, France
a2 CNRS UMR 5525, Medicine University, Faculté de Médecine, Domaine de la Merci, Université de Grenoble, 38700 La Tronche, France
Dietary cholesterol comes exclusively from animal sources, thus it is naturally present in our diet and tissues. It is an important component of cell membranes and a precursor of bile acids, steroid hormones and vitamin D. Contrary to phytosterols (originated from plants), cholesterol is synthesised in the human body in order to maintain a stable pool when dietary intake is low. Given the necessity for cholesterol, very effective intestinal uptake mechanisms and enterohepatic bile acid and cholesterol reabsorption cycles exist; conversely, phytosterols are poorly absorbed and, indeed, rapidly excreted. Dietary cholesterol content does not significantly influence plasma cholesterol values, which are regulated by different genetic and nutritional factors that influence cholesterol absorption or synthesis. Some subjects are hyper-absorbers and others are hyper-responders, which implies new therapeutic issues. Epidemiological data do not support a link between dietary cholesterol and CVD. Recent biological data concerning the effect of dietary cholesterol on LDL receptor-related protein may explain the complexity of the effect of cholesterol on CVD risk.
(Received June 30 2010)
(Revised November 11 2010)
(Accepted January 10 2011)
(Online publication March 09 2011)
Abbreviations: ABC, ATP-binding cassette; CETP, cholesteryl ester transfer protein; LRP, LDL receptor-related protein; NPC1L1, Niemann–Pick C1-like 1; PS, phytosterol