Abstract
BackgroundBio F1B hamster is an inbred hybrid strain that is highly susceptible to diet-induced atherosclerosis. We previously reported that feeding a high fat fish oil diet to Bio F1B hamster caused severe hyperlipidaemia. In this study we compared the effects of various diets in the Bio F1B hamster and the Golden Syrian hamster, which is an outbred hamster strain to investigate whether genetic background plays an important role in dietary fat mediated regulation of lipoprotein metabolism. We further investigated the mechanisms behind diet-induced hyperlipidaemia in F1B hamster.MethodsThe Bio F1B and Golden Syrian hamsters, 8 weeks old, were fed high fat diets rich in either monounsaturated fatty acids, an n-6: n-3 ratio of 5 or a fish oil diet for 4 weeks. Animals were fasted overnight and blood and tissue samples were collected. Plasma was fractionated into various lipoprotein fractions and assayed for triacylglycerol and cholesterol concentrations. Plasma lipoprotein lipase activity was measured using radioisotope method. Microsomal triglyceride transfer protein activity was measured in the liver and intestine. Plasma apolipoproteinB48, -B100 and apolipoprotein E was measured using Western blots. Two-way ANOVA was used to determine the effect of diet type and animal strain.ResultsThe fish oil fed F1B hamsters showed milky plasma after a 14-hour fast. Fish oil feeding caused accumulation of apolipoproteinB48 containing lipoprotein particles suggesting hindrance of triglyceride-rich lipoprotein clearance. There was no significant effect of diet or strain on hepatic or intestinal microsomal triglyceride transfer protein activity indicating that hyperlipidaemia is not due to an increase in the assembly or secretion of lipoprotein particles. F1B hamsters showed significantly reduced levels of lipoprotein lipase activity, which was inhibited by fish oil feeding.ConclusionEvidence is presented for the first time that alterations in lipoprotein lipase activity and mRNA levels contribute to varied response of these hamsters to dietary fat, highlighting the importance of genetic background in the regulation of lipid and lipoprotein metabolism by dietary fats. Bio F1B hamster may prove to be an important animal model to investigate nutrient mediated regulation of metabolic parameters under lipoprotein lipase deficiency.
Highlights
Bio F1B hamster is an inbred hybrid strain that is highly susceptible to diet-induced atherosclerosis
Animals in each strain were divided into one of three groups (n = 12, F1B; n = 12, Golden Syrian (GS)) and fed one of the three specified diets for a period of four weeks. These specified diets consisted of fat-free semi-purified diet (ICN biomedicals, Ohio, USA) supplemented with 200 g/kg (20% w/w) of either fish oil (FO) (Menhaden oil, Sigma-Aldrich, Ontario, Canada), high monounsaturated fatty acid (MUFA) safflower oil obtained from a local supermarket (MUFA), or a diet designed to give the animals an n-6:n-3 fatty acid ratio of ~5 (n6:n3)
We investigated the effects of diet and strain on Microsomal triglyceride transfer protein (MTTP) activity, which is involved in the formation of very-low density lipoproteins (VLDL) and chylomicrons from the liver and intestine respectively
Summary
Bio F1B hamster is an inbred hybrid strain that is highly susceptible to diet-induced atherosclerosis. Hypertriglyceridaemia arises mainly from alterations in lipid and lipoprotein metabolism that affect the clearance of TGrich lipoproteins, namely very-low density lipoproteins (VLDL) and chylomicrons This increase can be due to several factors; i.e. increased production and secretion of VLDL and chylomicrons from the liver and intestine respectively, a decrease in their hydrolysis by lipoprotein lipase (LPL) or hepatic uptake by the low-density lipoprotein (LDL) receptor. The subsequent development of hypertriglyceridaemia is detrimental to cardiovascular health as it promotes a decrease in high-density lipoprotein (HDL) concentrations, a simultaneous increase in LDL, and an increase in the prevalence of small, dense LDL particles. These factors are characteristic of an atherogenic lipoprotein phenotype that increases the risk for the onset of CVD [3,4]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
