期刊
MOLECULAR NUTRITION & FOOD RESEARCH
卷 60, 期 10, 页码 2198-2207出版社
WILEY
DOI: 10.1002/mnfr.201500930
关键词
apoE knock-out mice; Endothelial dysfunction; Liver; n-3 PUFA; Nitric oxide
资金
- FNRS (Fond National de la Recherche Scientifique, Belgium) [CDR J.0122.15]
- Walloon Region [1217802]
- FRS-FNRS [WELBIO-CR-2012S-02R]
- Funds InBev-Baillet Latour (Grant for Medical Research)
- ERC (European Research Council) [336452-ENIGMO]
- Excellence Walloon Region project (Food4Gut)
Scope: Western diets are characterized by low intake of n-3 PUFA compensated by constant amounts of n-6 PUFA. Reduced intake of n-3 PUFA is associated with increased cardiovascular risk, as observed in nonalcoholic fatty liver disease patients. The study aimed to evaluating the impact of dietary n-3 PUFA depletion on endothelial function, an early key event of cardiovascular diseases. Methods and results: C57Bl/6J or apolipoprotein E knock-out (apoE(-/-)) were fed control (CT) or n-3 PUFA-depleted diets (DEF) for 12 wks. Mice fed n-3 DEF diet developed a hepatic steatosis, linked to changes in hepatic expression of genes controlled by Sterol Regulatory Element Binding Protein-1 and -2. Vascular function was assessed on second-and third-order mesenteric arteries and n-3 PUFA-depleted apoE(-/-) mice presented endothelial dysfunction characterized by decreased vasorelaxation in response of acetylcholine. The presence of a nitric oxide synthase (NOS) inhibitor blunted the relaxation in each groups and heme-nitrosylated hemoglobin blood (Hb-NO) level was significantly lower in n-3 PUFA-depleted apoE(-/-) mice. Conclusion: Twelve weeks of n-3 DEF diet promote steatosis and accelerate the process of endothelial dysfunction in apoE(-/-) mice by a mechanism involving the NOS/NO pathway. We propose n-3 PUFA-depleted apoE(-/-) mice as a new model to study endothelial dysfunction related to hepatic steatosis independently of obesity.
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