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Bio F1B hamster: a unique animal model with reduced lipoprotein lipase activity to investigate nutrient mediated regulation of lipoprotein metabolism.

Cheema SK, Cornish ML - Nutr Metab (Lond) (2007)

Bottom Line: 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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Biochemistry, Memorial University, St, John's, NL, A1B 3X9, Canada. skaur@mun.ca.

ABSTRACT

Background: Bio 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.

Methods: The 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.

Results: The 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.

Conclusion: Evidence 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.

No MeSH data available.


Related in: MedlinePlus

The plasma lipid profile of F1B (solid) and Golden Syrian (GS) (shaded) hamsters. Hamsters were fed fish oil (FO), monounsaturated fatty acid rich (MUFA), and N6:N3 diets. The specified diets were fed for a period of four weeks. Fasting plasma samples were collected and analyzed for total plasma cholesterol (A), triglycerides (B), free cholesterol (C), and cholesterol esters (D) as described in the material and methods section. Values are means ± SEM (n = 6, F1B; n = 6, GS). Means for a variable with a different letter are significantly different (p = 0.05) by one-way ANOVA, and the Newman-Keuls post-hoc test after a significant interaction between diet and strain was found by two-way ANOVA.
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Figure 2: The plasma lipid profile of F1B (solid) and Golden Syrian (GS) (shaded) hamsters. Hamsters were fed fish oil (FO), monounsaturated fatty acid rich (MUFA), and N6:N3 diets. The specified diets were fed for a period of four weeks. Fasting plasma samples were collected and analyzed for total plasma cholesterol (A), triglycerides (B), free cholesterol (C), and cholesterol esters (D) as described in the material and methods section. Values are means ± SEM (n = 6, F1B; n = 6, GS). Means for a variable with a different letter are significantly different (p = 0.05) by one-way ANOVA, and the Newman-Keuls post-hoc test after a significant interaction between diet and strain was found by two-way ANOVA.

Mentions: The plasma from fish oil fed F1B hamsters was milky and packed with chylomicron-like particles (Figure 1), however milky plasma was not present in fish oil fed GS hamsters. Plasma total cholesterol (A), triglyceride (B), free cholesterol (C), and cholesterol ester (d) concentrations for F1B and GS hamsters on all three diets are shown in Figure 2. All lipid parameters were influenced by both diet and animal strain with a significant interaction between the two (P < 0.001). F1B hamsters on the fish oil diet had dramatically higher total plasma cholesterol concentrations (P < 0.001), TG concentrations (P < 0.001), FC concentrations (P < 0.001) and CE concentrations (P < 0.001) compared to F1B hamsters on the MUFA and n6:n3 diets. Fish oil fed GS hamsters had significantly higher total plasma cholesterol concentrations (P < 0.001) and plasma FC concentrations (P < 0.01) than the GS hamsters on the MUFA and n6:n3 diets. There was no significant effect of fish oil feeding however, on total plasma TG concentration or CE concentration in GS hamsters. While fish oil feeding significantly increased total plasma cholesterol and FC concentrations in both hamster strains, fish oil fed F1B hamsters had significantly higher concentrations of all lipid parameters (P < 0.001) than fish oil fed GS hamsters. Plasma cholesterol concentrations in F1B hamsters on the fish oil diet were 3 times that of fish oil fed GS hamsters. Similarly, plasma TG concentrations were 5 times greater in fish oil fed F1B hamsters when compared to GS hamsters. There was no significant difference between the MUFA and n6:n3 diets for plasma cholesterol, TG, FC, or CE concentrations in either F1B or GS hamsters.


Bio F1B hamster: a unique animal model with reduced lipoprotein lipase activity to investigate nutrient mediated regulation of lipoprotein metabolism.

Cheema SK, Cornish ML - Nutr Metab (Lond) (2007)

The plasma lipid profile of F1B (solid) and Golden Syrian (GS) (shaded) hamsters. Hamsters were fed fish oil (FO), monounsaturated fatty acid rich (MUFA), and N6:N3 diets. The specified diets were fed for a period of four weeks. Fasting plasma samples were collected and analyzed for total plasma cholesterol (A), triglycerides (B), free cholesterol (C), and cholesterol esters (D) as described in the material and methods section. Values are means ± SEM (n = 6, F1B; n = 6, GS). Means for a variable with a different letter are significantly different (p = 0.05) by one-way ANOVA, and the Newman-Keuls post-hoc test after a significant interaction between diet and strain was found by two-way ANOVA.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2235869&req=5

Figure 2: The plasma lipid profile of F1B (solid) and Golden Syrian (GS) (shaded) hamsters. Hamsters were fed fish oil (FO), monounsaturated fatty acid rich (MUFA), and N6:N3 diets. The specified diets were fed for a period of four weeks. Fasting plasma samples were collected and analyzed for total plasma cholesterol (A), triglycerides (B), free cholesterol (C), and cholesterol esters (D) as described in the material and methods section. Values are means ± SEM (n = 6, F1B; n = 6, GS). Means for a variable with a different letter are significantly different (p = 0.05) by one-way ANOVA, and the Newman-Keuls post-hoc test after a significant interaction between diet and strain was found by two-way ANOVA.
Mentions: The plasma from fish oil fed F1B hamsters was milky and packed with chylomicron-like particles (Figure 1), however milky plasma was not present in fish oil fed GS hamsters. Plasma total cholesterol (A), triglyceride (B), free cholesterol (C), and cholesterol ester (d) concentrations for F1B and GS hamsters on all three diets are shown in Figure 2. All lipid parameters were influenced by both diet and animal strain with a significant interaction between the two (P < 0.001). F1B hamsters on the fish oil diet had dramatically higher total plasma cholesterol concentrations (P < 0.001), TG concentrations (P < 0.001), FC concentrations (P < 0.001) and CE concentrations (P < 0.001) compared to F1B hamsters on the MUFA and n6:n3 diets. Fish oil fed GS hamsters had significantly higher total plasma cholesterol concentrations (P < 0.001) and plasma FC concentrations (P < 0.01) than the GS hamsters on the MUFA and n6:n3 diets. There was no significant effect of fish oil feeding however, on total plasma TG concentration or CE concentration in GS hamsters. While fish oil feeding significantly increased total plasma cholesterol and FC concentrations in both hamster strains, fish oil fed F1B hamsters had significantly higher concentrations of all lipid parameters (P < 0.001) than fish oil fed GS hamsters. Plasma cholesterol concentrations in F1B hamsters on the fish oil diet were 3 times that of fish oil fed GS hamsters. Similarly, plasma TG concentrations were 5 times greater in fish oil fed F1B hamsters when compared to GS hamsters. There was no significant difference between the MUFA and n6:n3 diets for plasma cholesterol, TG, FC, or CE concentrations in either F1B or GS hamsters.

Bottom Line: 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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Biochemistry, Memorial University, St, John's, NL, A1B 3X9, Canada. skaur@mun.ca.

ABSTRACT

Background: Bio 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.

Methods: The 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.

Results: The 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.

Conclusion: Evidence 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.

No MeSH data available.


Related in: MedlinePlus