Inulin Improves Postprandial Hypertriglyceridemia by Modulating Gene Expression in the Small Intestine

Abstract

Postprandial hyperlipidemia is an important risk factor for cardiovascular diseases in the context of obesity. Inulin is a non-digestible carbohydrate, known for its beneficial properties in metabolic disorders. We investigated the impact of inulin on postprandial hypertriglyceridemia and on lipid metabolism in a mouse model of diet-induced obesity. Mice received a control or a western diet for 4 weeks and were further supplemented or not with inulin for 2 weeks (0.2 g/day per mouse). We performed a lipid tolerance test, measured mRNA expression of genes involved in postprandial lipid metabolism, assessed post-heparin plasma and muscle lipoprotein lipase activity and measured lipid accumulation in the enterocytes and fecal lipid excretion. Inulin supplementation in western diet-fed mice decreases postprandial serum triglycerides concentration, decreases the mRNA expression levels of Cd36 (fatty acid receptor involved in lipid uptake and sensing) and apolipoprotein C3 (Apoc3, inhibitor of lipoprotein lipase) in the jejunum and increases fecal lipid excretion. In conclusion, inulin improves postprandial hypertriglyceridemia by targeting intestinal lipid metabolism. This work confirms the interest of using inulin supplementation in the management of dyslipidemia linked to obesity and cardiometabolic risk.

Keywords: inulin; obesity; postprandial hypertriglyceridemia.

Figure 1

Body weight evolution. Inulin supplementation was introduced after 4 weeks. Data are presented as mean ± SEM and analyzed with a mixed model ANOVA followed by Tukey post hoc test. * p < 0.05 versus CT, § p < 0.05 versus CT + I.

Figure 2

Serum triglyceride profile after olive oil load (A). Free fatty acid profile after olive oil load (B). Data are presented as mean ± SEM and analyzed with a mixed model ANOVA followed by Tukey post hoc tests. * p < 0.05 versus CT, § p < 0.05 versus CT + I, † p < 0.05 versus WD.

Figure 3

mRNA relative expression of genes involved in fatty acid absorption in the jejunum. Data are presented as mean ± SEM and analyzed with two-way ANOVA followed by Tukey post hoc tests. * p < 0.05 versus CT, § p < 0.05 versus CT + I, † p < 0.05 versus WD.

Figure 4

Fecal lipid content. Data are presented as mean ± SEM and analyzed with two-way ANOVA followed by Tukey post hoc tests. * p < 0.05 versus CT, § p < 0.05 versus CT + I, † p < 0.05 versus WD.

Figure 5

Lpl mRNA expression in the muscle and subcutaneous adipose tissue (A). Level of mRNA expression of post-translational regulators of LPL activity (B). Data are presented as mean ± SEM and analyzed with two-way ANOVA followed by Tukey post hoc tests. * p < 0.05 versus CT, § p < 0.05 versus CT + I, † p < 0.05 versus WD.

Figure 6

Liver lipid content (A). Quantification of hepatic lipid staining with oil red O (B). Level of mRNA expression of Mttp and Apob, involved in VLDL synthesis in the liver (C). Level of mRNA expression of remnant receptors Lrp1, Ldlr and Sdc1 in the liver (D). Data are presented as mean ± SEM and analyzed with two-way ANOVA followed by Tukey post hoc tests. * p < 0.05 versus CT, § p < 0.05 versus CT + I.