Other sites of control

HMG-CoA reductase fimctions as the major control point for sterol biosynthesis under most physiological conditions. However, regulation is not achieved solely through changes in the quantity and activity of HMG-CoA reductase. Several other enzymes are also subject to and function in regulatory control. 

Alterations in the levels of each of the enzymes of the early, or common portion of the sterol/isoprenoid biosynthetic pathway (acetyl-CoA isopentenyl pyrophosphate) have been observed in response to certain physiological stimuli. These alterations usually parallel those in HMG-CoA reductase. For example  

In at least one circumstance, however, sterol/isoprenoid biosynthesis is regulated by mechanisms independent of HMG-CoA reductase. When HeLa cells are exposed to dexamethasone, sterol biosynthesis and HMG-CoA synthase activity decrease. 

To summarize, it appears that some regulatory control is exerted over several enzymes of the early portion of the sterol/isoprenoid biosynthetic pathway. The changes in these early enzymes usually parallel those in HMG-CoA reductase and probably represent a cellular conservation process rather than a mechanism for biosynthetic control [82]. The temporal relationship between the change in HMG-CoA reductase activity and that of other early enzymes when CHO cells are incubated in delipidated medium supports this hypothesis [210]. However, it also appears that, under certain circumstances, regulation of these enzymes can serve as a mechanism for control of sterol biosynthesis. 

Reactions in the sterol/isoprenoid biosynthetic pathway located after the branch point intermediate farnesyl pyrophosphate regulate the distribution of common precursor molecules. Examples include  

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