Dietary fat saturation effects on low-density-lipoprotein concentrations and metabolism in various animal models.

Saturated vegetable oils (coconut, palm, and palm kernel oil) and fats (butter and lard) are hypercholesterolemic relative to monounsaturated and polyunsaturated vegetable oils. The increase in plasma low-density-lipoprotein-cholesterol (LDL-C) concentrations associated with consumption of saturated vegetable oils and fats is largely explained by a decrease in hepatic LDL receptor activity and an increase in the LDL-C production rate. Hepatic LDL receptor activity may be regulated by the messenger RNA concentration of the LDL receptor. The decrease in hepatic LDL receptor activity with saturated fat feeding is associated with decreased hepatic sterol O-acyltransferase activity and, therefore, a reduced inert pool of cholesteryl ester. A putative regulatory pool of cholesterol is increased with saturated fat feeding and suppresses LDL receptor activity, possibly through hepatic messenger RNA regulation. For most studies, an independent effect of a vegetable oil or fat could not be ascertained because there was no neutral control and at least two of the test oils or fats were varied. Animal data for the effects of individual fatty acids on plasma LDL-C concentrations and metabolism are sparse. The evidence suggests that caproic acid (6:0), caprylic acid (8:0), and capric acid (10:0) are neutral with respect to their LDL-C-raising properties and their ability to modulate LDL metabolism. Lauric acid (12:0), myristic acid (14:0), and palmitic acid (16:0) are approximately equivalent in their LDL-C-raising potential by reducing hepatic LDL receptor activity and increasing the LDL-C production rate, apparently via modulation of sterol O-acyltransferase activity. Stearic acid (18:0) appears to be neutral in its LDL-C-raising potential and how it affects LDL metabolism.