Rate limiting enzyme in cholesterol synthesis ..

The synthesis of HMG-CoA is also regulated by the level of cholesterol (see below).

Biosynthesis of Lipids | Cholesterol | Biosynthesis

Table 2 shows the effects of overexpression of various SREBP genes on cholesterol and fatty acid synthesis, and on liver cholesterol and triglyceride content; note that a value of 1 represents wild-type levels, while a value above 1 represents higher-than-wild-type levels

T1 - Cloning and regulation of cholesterol 7α-hydroxylase, the rate-limiting enzyme in bile acid biosynthesis

the first fatty acids ester which is a rate-limiting step

Table1 shows that cholesterol and fatty acid synthetic activity, as well as livertriglyceride content, declined from wild-type levels in all transgenic micethat survived into adulthood. Liver cholesterol content increased in SREBP-1cknockouts, declined in SCAP inactivated mice and SREBP-1a/1c double knockouts, and was unchanged in S1P-inactivated mice.

By slowing the rate of the rate-limiting step, statins decrease the overall rate of cholesterol synthesis.

The expression of genes that encode proteins involved in the synthesis of cholesterol (HMG-CoA reductase) and uptake of cholesterol (LDL receptor) is regulated by the sterol response element binding protein (SREBP).

Cholesterol regulates the activity of SREBP. When initially synthesized, SREBP is a membrane protein that resides in the ER.