I stand corrected. What I should have said was that increased fat intake, increases cholesterol production.
Regulation of cholesterol synthesis by dietary fat and cholesterol
Cholesterol is an essential component of mammalian membranes and a precursor for bile acids, vitamin D and steroid hormones. Up to now, a lot of studies have been done to determine the effect of dietary factors on circulating cholesterol concentrations in humans, since elevated plasma total cholesterol and LDL-cholesterol have proved to be closely related to atherosclerosis and coronary heart disease (1). Dietary cholesterol and saturated fatty acids (SFAs) increase serum cholesterol concentrations, while polyunsaturated fatty acids (PUFAs) lower cholesterol concentrations. Monounsaturated fatty acids (MUFAs) decrease serum total and LDL cholesterol concentrations but have no effect on HDL cholesterol (2,3). However, how dietary fat and cholesterol affect cholesterol synthesis and whether this contributes to their effect on circulating cholesterol concentrations remains unresolved. The purpose of this paper is to review studies examining the effects of diets containing different amounts of fat and cholesterol on cholesterol synthesis. Also considered, is whether reductions or elevations in cholesterol synthesis is responsible for changes observed in cholesterol concentrations affected by diets. The de novo cholesterol synthesis pathway and several methods for cholesterol synthesis measurement in human will be discussed in this paper.
The inputs of whole-body cholesterol pool are mainly from diet and de novo synthesis.
Endogenous cholesterol synthesis accounts for two-thirds of the cholesterol input at the whole-body level, which is about 1 g of cholesterol each day (4). The primary site of de novo cholesterol synthesis is the liver, although extrahepatic tissues such as small intestine, adrenal cortex, ovaries and testes also synthesize cholesterol for various uses. Cholesterol synthesis requires acetyl CoA, ATP, the reduced form of nicotinamide-adenine dinucleotide phosphate (NADPH), and oxygen (4). HMG CoA reductase, catalyzing the NADPH-dependent reduction of HMG CoA to mevalonic acid, is the rate-limiting enzyme in this pathway. Squalene and lanosterol are both 30-carbon precursors of cholesterol, and the difference between these compounds is that squalene is a linear precursor of cholesterol and lanosterol is converted from squalene through oxidation and cyclization reactions.
Nautica