Shen Wan, Wolf Patricia G, Carbonero Franck, Zhong Wei, Reid Tanya, Gaskins H Rex, McIntosh Michael K
Department of Nutrition, University of North Carolina, Greensboro, NC.
Institute of Genomic Biology, University of Illinois, Urbana-Champaign, IL.
J Nutr. 2014 Aug;144(8):1181-7. doi: 10.3945/jn.114.194332. Epub 2014 Jun 11.
Recent studies have highlighted the relation between high-fat (HF) diets, the gut microbiota, and inflammation. However, the role of sulfidogenic bacteria in mediating these effects has been explored only recently. Therefore, we tested the hypothesis that an HF diet rich in saturated fat stimulates sulfidogenic bacteria and that these increases correlate with intestinal and systemic inflammatory responses. Forty C57BL/6J male mice were fed a low-fat (LF; 10% of energy) or an HF lard-based (60% of energy) diet for 6 or 20 wk. Mucosa samples were collected from the ileum, cecum, and colon and used for measuring 16S ribosomal RNA and functional genes of sulfidogenic bacteria. Matching intestinal samples and visceral and subcutaneous white adipose tissue (WAT) depots were used to measure mRNA abundance for inflammatory genes. Mice fed the HF diet had greater (P < 0.05) abundance of 3 types of sulfidogenic bacteria, primarily in colonic mucosa, compared with LF-fed mice at week 20. Although HF feeding did not increase intestinal inflammation at week 6, ileal markers of macrophage infiltration and inflammation were upregulated (P < 0.05) 1- to 6-fold at week 20. HF feeding impaired the localization of the tight junction protein zonula occludens 1 at the apical area of the ileal epithelium at weeks 6 and 20. Mice fed the HF diet had 1- to 100-fold greater (P < 0.05) mRNA levels of markers of macrophage infiltration in visceral and subcutaneous WAT at week 20, but not at week 6, compared with LF-fed mice. These results provide evidence that chronic, but not acute, consumption of an HF lard-based diet may be linked with pathways of microbial metabolism that potentially contribute to chronic intestinal and systemic inflammation. Such linkage provides further support for reducing consumption of saturated fats.
近期研究强调了高脂(HF)饮食、肠道微生物群和炎症之间的关系。然而,产硫化氢细菌在介导这些效应中的作用直到最近才被探讨。因此,我们检验了以下假设:富含饱和脂肪的HF饮食会刺激产硫化氢细菌,且这些细菌数量的增加与肠道和全身炎症反应相关。将40只C57BL/6J雄性小鼠分为两组,分别喂食低脂(LF;能量的10%)或基于猪油的HF饮食(能量的60%),持续6周或20周。从回肠、盲肠和结肠收集黏膜样本,用于测量产硫化氢细菌的16S核糖体RNA和功能基因。使用匹配的肠道样本以及内脏和皮下白色脂肪组织(WAT)库来测量炎症基因的mRNA丰度。与喂食LF饮食的小鼠相比,在第20周时,喂食HF饮食的小鼠体内3种产硫化氢细菌的丰度更高(P<0.05),主要存在于结肠黏膜中。虽然在第6周时,HF饮食并未增加肠道炎症,但在第20周时,回肠中巨噬细胞浸润和炎症的标志物上调了1至6倍(P<0.05)。在第6周和第20周时,HF饮食均破坏了紧密连接蛋白闭合蛋白1在回肠上皮顶端区域的定位。与喂食LF饮食的小鼠相比,在第20周而非第6周时,喂食HF饮食的小鼠在内脏和皮下WAT中巨噬细胞浸润标志物的mRNA水平高1至100倍(P<0.05)。这些结果表明,长期而非短期食用基于猪油的HF饮食可能与微生物代谢途径有关,这可能会导致慢性肠道和全身炎症。这种联系为减少饱和脂肪的摄入提供了进一步的支持。