The first three control mechanisms are exerted by cholesterol itself. Cholesterol acts as a feed-back inhibitor of pre-existing HMGR as well as inducing rapid degradation of the enzyme. The latter is the result of cholesterol-induced polyubiquitination of HMGR and its degradation in the proteosome (see proteolytic degradation below). This ability of cholesterol is a consequence of the sterol sensing domain, SSD of HMGR. In addition, when cholesterol is in excess the amount of mRNA for HMGR is reduced as a result of decreased expression of the gene. The mechanism by which cholesterol (and other sterols) affect the transcription of the HMGR gene is described below under regulation of sterol content .
Nope. The mainstream media portrayal of cholesterol’s health effects is about as accurate as the claim of most Olympians that they’re natural. The media will have you believe all that cholesterol you consume ends up clogging your arteries, but the reality is, for most people how much cholesterol you consume in your diet does not even influence how much cholesterol is in your blood . Cholesterol is so important for the body that it is highly regulated. If your diet does not contain much cholesterol, your intestines will increase their absorption to compensate. If that’s not enough, your body will produce its own cholesterol.