Abstract
BackroundWestern diet is characterized by an insufficient n-3 polyunsaturated fatty acid (PUFA) consumption which is known to promote the pathogenesis of several diseases. We have previously observed that mice fed with a diet poor in n-3 PUFA for two generations exhibit hepatic steatosis together with a decrease in body weight. The gut microbiota contributes to the regulation of host energy metabolism, due to symbiotic relationship with fermentable nutrients provided in the diet. In this study, we have tested the hypothesis that perturbations of the gut microbiota contribute to the metabolic alterations occurring in mice fed a diet poor in n-3 PUFA for two generations (n-3/- mice).MethodsC57Bl/6J mice fed with a control or an n-3 PUFA depleted diet for two generations were supplemented with prebiotic (inulin-type Fructooligosaccharides, FOS, 0.20 g/day/mice) during 24 days.Resultsn-3/-mice exhibited a marked drop in caecum weight, a decrease in lactobacilli and an increase in bifidobacteria in the caecal content as compared to control mice (n-3/+ mice). Dietary supplementation with FOS for 24 days was sufficient to increase caecal weight and bifidobacteria count in both n-3/+ and n-3/-mice. Moreover, FOS increased lactobacilli content in n-3/-mice, whereas it decreased their level in n-3/+ mice. Interestingly, FOS treatment promoted body weight gain in n-3/-mice by increasing energy efficiency. In addition, FOS treatment decreased fasting glycemia and lowered the higher expression of key factors involved in the fatty acid catabolism observed in the liver of n-3/-mice, without lessening steatosis.Conclusionsthe changes in the gut microbiota composition induced by FOS are different depending on the type of diet. We show that FOS may promote lactobacilli and counteract the catabolic status induced by n-3 PUFA depletion in mice, thereby contributing to restore efficient fat storage.
Highlights
Dietary n-3 polyunsaturated fatty acids (PUFA) have received considerable attention during the last decades
C57Bl/6J mice fed with a control or an n-3 PUFA depleted diet for two generations were supplemented with prebiotic during 24 days
In conclusion, a low n-3 PUFA dietary consumption is associated to metabolic alterations that target the liver, leading to steatosis
Summary
Dietary n-3 polyunsaturated fatty acids (PUFA) have received considerable attention during the last decades. Many epidemiological and clinical studies have described the beneficial effects of these fatty acids on cardiovascular disease [1], inflammation [2,3], insulin sensitivity [4,5] and hypertriglyceridemia [6]. By their ability to modulate the expression of regulatory. The hepatic mRNA content of fatty acid synthase (FAS)-the rate-limiting enzyme for lipid synthesis-was decreased, whereas carnitine palmitoyl transferase 1 (CPT1) and peroxisome proliferator-activated receptor gamma coactivator a (PGC1a)-two key factors involved in b-oxidation-were increased, suggesting catabolic alterations of the energy homeostasis in the liver tissue of n-3 PUFA depleted mice [21]
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