Jb. Dictenberg et al., HYPERLIPIDEMIC EFFECTS OF TRANS-FATTY-ACIDS ARE ACCENTUATED BY DIETARY-CHOLESTEROL IN GERBILS, Journal of nutritional biochemistry, 6(7), 1995, pp. 353-361
Trans isomers of dietary fatty acids, generated during the commercial
hydrogenation of unsaturated fats, may contribute to coronary heart di
sease (CHD) in humans by interfering with lipid metabolism. To examine
this possibility in a fat-sensitive model, the Mongolian gerbil (Meri
ones unguiculatus) was used to compare the cholesterolemic and triglyc
eridemic potential of modest increments of trans fatty acids from part
ially hydrogenated soybean oil with other saturated fatty acids in the
presence and absence of dietary cholesterol. Age-, dose-, and time-de
pendent effects were examined in weanling, 6-month-old, and 1-year-old
gerbils. Although lipoprotein metabolism in weanling gerbils was init
ially refractory to trans fat, even as perturbations by saturated fatt
y acids were demonstrable, these gerbils eventually (after 16 weeks) d
eveloped a trans-induced hypercholesterolemia that was intermediate be
tween the response to 16:0 and 12:0 + 14:0. The hepatic and plasma 18:
1/18:2 cholesteryl ester (CE) ratio was depressed by trans in a manner
similar to saturated fatty acids. The 6-month-old gerbils readily dev
eloped hypertriglyceridemia but not hypercholesterolemia, again reveal
ing a decrease in the plasma 18:1/18:2 CE ratio. The 1-year-old gerbil
s revealed a dose-related (0, 5, 10%en as trans) elevation in total ch
olesterol (TC), and especially triglycerides (TG), that was accentuate
d by 0.04% dietary cholesterol. Increases in plasma lipids were again
accompanied by a significant decrease in the mass of hepatic esterifie
d cholesterol, particularly 18:1-cholesteryl esters. Thus, dietary tra
ns-fatty acids induce age-, time-, and dose-dependent modulations in g
erbil plasma lipids associated with decreased 18:1 cholesteryl esters.
Further investigation with gerbils may reveal mechanisms by which tra
ns fat consumption disturbs lipoprotein metabolism.