Dietary cholesterol reduces lipoprotein lipase activity in the atherosclerosis-susceptible Bio F₁B hamster

Abstract

We have compared lipoprotein metabolism in, and susceptibility to atherosclerosis of, two strains of male Golden Syrian hamster, the Bio F 1 B hybrid and the dominant spot normal inbred (DSNI) strain. When fed a normal low-fat diet containing approximately 40 g fat and 0·3 g cholesterol/kg, triacylglycerol-rich lipoprotein (chylomicron þ VLDL) and HDL-cholesterol were significantly higher (P,0·001) in Bio F 1 B hamsters than DSNI hamsters. When this diet was supplemented with 150 g coconut oil and either 0·5 or 5·0 g cholesterol/kg, significant differences were seen in response. In particular, the high-cholesterol diet produced significantly greater increases in plasma cholesterol and triacylglycerol in the Bio F 1 B compared with the DSNI animals (P¼ 0·002 and P,0·001 for cholesterol and triacylglycerol, respectively). This was particularly dramatic in non-fasting animals, suggesting an accumulation of chylomicrons. In a second experiment, animals were fed 150 g coconut oil/kg and 5·0 g cholesterol/kg for 6 and 12 months. Again, the Bio F 1 B animals showed dramatic increases in plasma cholesterol and triacylglycerol, and this was confirmed as primarily due to a rise in chylomicron concentration. Post-heparin lipoprotein lipase activity was significantly reduced (P,0·001) in the Bio F 1 B compared with the DSNI animals at 6 months, and virtually absent at 12 months. Bio F 1 B animals were also shown to develop significantly more (P,0·001) atherosclerosis. These results indicate that, in the Bio F 1 B hybrid hamster, cholesterol feeding reduces lipoprotein lipase activity, thereby causing the accumulation of chylomicrons that may be associated with their increased susceptibility to atherosclerosis. The male Golden Syrian hamster has been used extensively in studies of lipoprotein metabolism because it is more similar in this respect to man than other rodent species. It has also proven to be a useful model in studying pharmacological (Kowala et al.

Diets Enriched in Fish-Oil or Seal-Oil have Distinct Effects on Lipid Levels and Peroxidation in BioF1B Hamsters

“…We investigated the metabolic actions of dietary seal-oil as compared to fish-oil under conditions of low LPL activity as found in the BioF 1 B hamster. BioF 1 B hamster, a hybrid strain, is genetically susceptible to diet-induced hyperlipidemia and atherosclerosis 22,23. We report, for the first time, that in contrast to the feeding of a high fat diet with fish-oil, feeding seal-oil did not cause milky plasma after an overnight fast.…”

“…Elevated plasma apoB48 expression in fish-oil-fed BioF 1 B hamsters even after a 14 h fast indicated the presence of lower-density lipoproteins, seen as milky plasma, which was absent in seal-oil-fed BioF 1 B hamsters. Reduced post-heparin LPL activity was previously shown to be associated with an increased accumulation of chylomicron-like particles in BioF 1 B hamsters 16,23. Overall, a combined effect of low LPL activity and differences in positional distribution of n-3 PUFAs may have resulted in milky plasma in hamsters fed with fish-oil.…”

Use of hamster as a model to study diet-induced atherosclerosis

“…Intervention periods ranged from 3 weeks [59,60] to 12 months [22,61]. The most common intervention periods ranged from 10 and 12 weeks [33-35,37,42,43,46,48,51,53-56,62-66].…”

Critical evaluation of normotensive rats as models for hypercholesterolaemia-induced atherosclerosis

“…For example, severe hypercholesterolaemia was induced in rats (Pisulewski et al, 2002;Vasconen et al, 2002) and more recently in atherosclerosis susceptible F 1 B hybrid hamsters (McAteer et al, 2003;Ntianos et al, 2003) fed hypercholesterolaemic diets. However, it should be stressed that hypercholesterolaemia in rats may be induced only by high-fat and highcholesterol diets containing cholic acid.…”