Dietary myristic, palmitic, and linoleic acids modulate cholesterolemia in gerbils

Previous studies with cebus monkeys and review of published human data indicated that 85% to 90% of the variation in plasma cholesterol (TC) could be explained on the basis of dietary myristic (14:0) and linoleic (18:2) acid intake in the absence of cholesterol, and that 16:0 contributed to cholesterolemia as dietary cholesterol was increased. Because monkeys are a limited resource, a more convenient, sensitive model was sought for investigating these dietary fatty acid and plasma lipid relationships. Accordingly, this report describes the results of multiple regression analysis of the TC response to dietary fatty acids based on 319 young, male Mongolian gerbils fed a total of 59 purified diets supplying about 40% energy as fat from single or blended fat sources. Gerbils (6-16 animals per dietary group) were fed purified diets (21 with 0.01 to 0.08% cholesterol and 38 cholesterol-free) for 4-week periods. When cholesterol-free diets were fed, dietary 14:0 and 18:2 together accounted for 89% of the observed variation in TC. Although 14:0 consumption increased TC in a linear manner, the independent ability of 18:2 to lower cholesterol was nonlinear and exhibited a threshold effect at 5-6% dietary energy, above which further lowering of TC was less remarkable. In gerbils consuming cholesterol-supplemented diets, 87% of the observed variation in TC could be accounted for by a regression equation that included 14:0, palmitic acid (16:0), and a log function of 18:2 plus dietary cholesterol itself. These results demonstrate the applicability of gerbils for such studies and confirm previous observations in monkeys and humans that dietary 14:0 and 18:2 are the main fatty acids modulating plasma cholesterol under normocholesterolemic circumstances (i.e., when consuming low-cholesterol diets and lipoprotein metabolism is normal) whereas 16:0 also appears modestly hypercholesterolemic when LDL receptors are compromised (i.e., when dietary cholesterol or certain metabolic factors have encumbered lipoprotein metabolism).