Interaction of dietary cholesterol and triglycerides in the regulation of hepatic low density lipoprotein transport in the hamster.

Abstract

These studies report the effects of dietary cholesterol and triglyceride on rates of receptor-dependent and receptor-independent LDL transport in the liver of the hamster. In animals fed diets enriched with 0.1, 0.25, or 1% cholesterol for 1 mo, receptor-dependent LDL transport in the liver was suppressed by 43, 63, and 77%, respectively, and there were reciprocal changes in plasma LDL-cholesterol concentrations. In addition, dietary triglycerides modified the effect of dietary cholesterol on hepatic LDL transport and plasma LDL concentrations so that at each level of cholesterol intake, polyunsaturated triglycerides diminished and saturated triglycerides accentuated the effect of dietary cholesterol. When animals were raised from weaning on diets containing small amounts of cholesterol, the decline in receptor-dependent LDL transport was nearly abolished by the addition of polyunsaturated or monounsaturated triglycerides, but was markedly augmented by the addition of saturated lipids. When animals raised on diets containing cholesterol and saturated triglycerides were returned to the low cholesterol, low triglyceride control diet, hepatic receptor-dependent LDL transport and plasma LDLcholesterol concentrations returned essentially to normal within 2 wk. Neither receptor-independent LDL transport nor the receptor-dependent uptake of asialofetuin was significantly altered by dietary cholesterol or triglyceride suggesting that the effect of these lipids on hepatic LDL receptor activity was specific and not due to a generalized alteration in the physiochemical properties of hepatic membranes. These studies demonstrate the important role of saturated triglycerides in augmenting the effect of cholesterol in suppressing hepatic LDL receptor activity and elevating LDL-cholesterol levels.

Increasing amounts of dietary myristic acid modify the plasma cholesterol level and hepatic mass of Scavenger receptor BI without affecting bile acid biosynthesis in hamsters

“…In the present study, different levels of myristic acid (0.03 to 4.2%) do not alter the biosynthesis of bile acids or that of cholesterol since no differences in the HMGCoA activity of the different dietary groups was detected. These last data are similar to those found in previous studies [2,38].…”

“…close to that found in mammalian milks). The hamster is an animal model which has a well-established similarity with human cholesterol metabolism [37] and is sensitive to changes in the composition of dietary fats [20,25,38].…”

Effect of Various Dietary Fatty Acid Ethyl Esters on Plasma Cholesterol and Lipoprotein Metabolism in Rats.

“…These findings are consistent with data on hamsters: Spady and Dietschy [28,29] reported that when olive oil was partially replaced by tripalmitin, whole liver receptor-dependent LDL transport declined significantly and the plasma LDL concentration increased. In contrast, unsaturated triglycerides largely prevented the deleterious effect of dietary cholesterol on these parameters of hepatic metabolism.…”

Inability to fully suppress sterol synthesis rates with exogenous sterol in embryonic and extraembyronic fetal tissues

“…To gain a better understanding of the regulation of sterol biosynthesis during this rapid time of growth, the relationship between cholesterol concentrations and sterol synthetic rates in the fetal liver and body, the placenta, and the yolk sac were compared to the same relationship in the non-pregnant adult liver of the Golden Syrian hamster. Hamsters were used in these studies because 1) hamsters are readily responsive to dietary cholesterol [14,28], 2) embryonic and extraembryonic fetal tissue cholesterol concentrations can be readily changed in hamsters [29] and 3) the gestational age of hamsters is very precise [29]. We found that sterol synthesis rates were maximally suppressed in the adult liver but only marginally suppressed in each of the extraembryonic and embryonic fetal tissues in the presence of excess tissue cholesterol.…”