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Phytosterolaemia,1 causing severe atherosclerosis,2 illustrates the stringent requirements for sterols in membranes and the impact of low-density lipoprotein (LDL) receptor on metabolism, but is not associated with malformations seen with sterol biosynthetic defects.
Membranes contain hopanoids3 in bacteria and a range of phytosterols in plants, mostly campesterol and beta-sitosterol. Animal cell membranes contain cholesterol. The rate-controlling step in sterol biosynthesis is the formation of mevalonic acid by hydroxymethylglutaryl coenzyme A reductase that can be inhibited by statins. During biosynthesis six isopentenyl units form a 30-carbon molecule. Demethylation, double-bond reduction and the creation of one final unsaturated bond deliver cholesterol. Phytosterols are synthesised similarly but retain methyl or ethyl moieties or double bonds. Cholesterol evolved …
Handling editor Tahir S Pillay.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent Not required.
Provenance and peer review Commissioned; internally peer reviewed.
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