Key result
Inulin lowers postprandial triglycerides and increases fecal lipid excretion in western diet-fed mice.
Why the study?
Postprandial hyperlipidemia is an important cardiovascular risk factor in obesity, and the effects of inulin on postprandial hypertriglyceridemia and intestinal lipid metabolism were investigated.
Does inulin supplementation improve postprandial hypertriglyceridemia in a mouse model of diet-induced obesity?
Does inulin supplementation improve postprandial hypertriglyceridemia in a mouse model of diet-induced obesity?
Inulin supplementation improves postprandial hypertriglyceridemia by targeting intestinal lipid metabolism in a mouse model of diet-induced obesity.
Inulin lowered postprandial triglycerides in obese mice; leaves open translation to human cardiometabolic risk management.
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.
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Hiel et al. (2018) studied Diet-induced obesity and postprandial hypertriglyceridemia. Inulin vs. No inulin supplementation was evaluated on Postprandial serum triglycerides concentration, mRNA expression levels of Cd36 and Apoc3, and fecal lipid excretion. Inulin supplementation in western diet-fed mice decreased postprandial serum triglycerides, reduced jejunal Cd36 and Apoc3 mRNA expression, and increased fecal lipid excretion.
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