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.

Highlights

  • According to the World Health Organization (WHO), cardiovascular diseases (CVDs) are the first cause of death since an estimated 17.7 million people died from CVDs in 2015

  • We demonstrate the beneficial effect of ITF supplementation on hypertriglyceridemia after an acute fat load in the context of diet-induced obesity, and we propose new mechanisms highlighting the role of inulin on the expression of genes controlling lipid metabolism at the intestinal level

  • The cecal tissue weight was increased with inulin supplementation, whereas the cecal content was increased in western diet group (WD) + I versus WD and control group (CT) groups (Table 1)

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Summary

Introduction

According to the World Health Organization (WHO), cardiovascular diseases (CVDs) are the first cause of death since an estimated 17.7 million people died from CVDs in 2015. As part of the metabolic syndrome (MetS), dyslipidemia linked to obesity is an important risk factor for developing. A dyslipidemic profile includes hypertriglyceridemia, low HDL level and elevated level of LDL particles [1,2]. Among these factors, non-fasting triglycerides have been increasingly proposed as an important marker of the cardiovascular risk [3,4]. The human body is exposed to circulating. Studying postprandial lipemia in humans is hampered because of the lack of standardized methodology, and because multiple factors affect the postprandial response such as genetic factors, lifestyle and physiological and pathological conditions [5,6]. Diet composition plays a key role, more precisely depending on the type and amount of fat, carbohydrates, proteins, and fibers [6]

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