Metabolism and Nutrition Research Group, Louvain Drug Research Institute, Université catholique de Louvain, Brussels, Belgium.
Nutr Metab (Lond). 2011 Jun 27;8(1):44. doi: 10.1186/1743-7075-8-44.
Western 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).
C57Bl/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.
n-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.
the 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.
西方饮食的特点是 n-3 多不饱和脂肪酸(PUFA)摄入不足,已知这会促进多种疾病的发病机制。我们之前观察到,连续两代食用 n-3 PUFA 缺乏饮食的小鼠表现出肝脂肪变性,同时体重下降。肠道微生物群通过与饮食中提供的可发酵营养物质的共生关系,有助于调节宿主的能量代谢。在这项研究中,我们检验了这样一个假设,即肠道微生物群的紊乱导致连续两代食用 n-3 PUFA 缺乏饮食的小鼠发生代谢改变(n-3/- 小鼠)。
连续两代食用对照或 n-3 PUFA 耗尽饮食的 C57Bl/6J 小鼠在 24 天内补充益生元(菊粉型低聚果糖,FOS,0.20 g/天/只)。
与对照小鼠(n-3/+ 小鼠)相比,n-3/- 小鼠的盲肠重量明显下降,盲肠内容物中的乳杆菌减少,双歧杆菌增加。24 天的 FOS 饮食补充足以增加 n-3/+ 和 n-3/- 小鼠的盲肠重量和双歧杆菌计数。此外,FOS 增加了 n-3/- 小鼠的乳杆菌含量,而降低了 n-3/+ 小鼠的乳杆菌含量。有趣的是,FOS 治疗通过提高能量效率促进 n-3/- 小鼠体重增加。此外,FOS 治疗降低了 n-3/- 小鼠的空腹血糖,并降低了肝脏中观察到的与脂肪酸分解代谢相关的关键因子的高表达,而没有减轻脂肪变性。
FOS 引起的肠道微生物群组成的变化取决于饮食的类型。我们表明,FOS 可能促进乳杆菌的生长,并抵消 n-3 PUFA 缺乏引起的分解代谢状态,从而有助于恢复有效的脂肪储存。