Volynets Valentina, Louis Sandrine, Pretz Dominik, Lang Lisa, Ostaff Maureen J, Wehkamp Jan, Bischoff Stephan C
Department of Nutritional Medicine, University of Hohenheim, Stuttgart, Germany.
University of Colorado Anschutz Medical Campus, Denver, CO; and.
J Nutr. 2017 May;147(5):770-780. doi: 10.3945/jn.116.242859. Epub 2017 Mar 29.
The consumption of a Western-style diet (WSD) and high fructose intake are risk factors for metabolic diseases. The underlying mechanisms are largely unclear. To unravel the mechanisms by which a WSD and fructose promote metabolic disease, we investigated their effects on the gut microbiome and barrier function. Adult female C57BL/6J mice were fed a sugar- and fat-rich WSD or control diet (CD) for 12 wk and given access to tap water or fructose-supplemented water. The microbiota was analyzed with the use of 16S rRNA gene sequencing. Barrier function was studied with the use of permeability tests, and endotoxin, mucus thickness, and gene expressions were measured. The WSD increased body weight gain but not endotoxin translocation compared with the CD. In contrast, high fructose intake increased endotoxin translocation 2.6- and 3.8-fold in the groups fed the CD + fructose and WSD + fructose, respectively, compared with the CD group. The WSD + fructose treatment also induced a loss of mucus thickness in the colon (-46%) and reduced defensin expression in the ileum and colon. The lactulose:mannitol ratio in the WSD + fructose mice was 1.8-fold higher than in the CD mice. Microbiota analysis revealed that fructose, but not the WSD, increased the Firmicutes:Bacteroidetes ratio by 88% for CD + fructose and 63% for WSD + fructose compared with the CD group. abundance was greater in the WSD mice than in the CD mice (63-fold) and in the WSD + fructose mice than in the CD + fructose mice (330-fold). The consumption of a WSD or high fructose intake differentially affects gut permeability and the microbiome. Whether these differences are related to the distinct clinical outcomes, whereby the WSD primarily promotes weight gain and high fructose intake causes barrier dysfunction, needs to be investigated in future studies.
食用西式饮食（WSD）和高果糖摄入是代谢性疾病的危险因素。其潜在机制在很大程度上尚不清楚。为了阐明WSD和果糖促进代谢性疾病的机制，我们研究了它们对肠道微生物群和屏障功能的影响。成年雌性C57BL/6J小鼠喂食富含糖和脂肪的WSD或对照饮食（CD）12周，并给予自来水或补充果糖的水。使用16S rRNA基因测序分析微生物群。通过通透性测试研究屏障功能，并测量内毒素、黏液厚度和基因表达。与CD相比，WSD增加了体重增加，但未增加内毒素易位。相比之下，与CD组相比，高果糖摄入分别使喂食CD + 果糖和WSD + 果糖组的内毒素易位增加了2.6倍和3.8倍。WSD + 果糖处理还导致结肠黏液厚度减少（-46%），并降低回肠和结肠中防御素的表达。WSD + 果糖小鼠的乳果糖：甘露醇比值比CD小鼠高1.8倍。微生物群分析显示，与CD组相比，果糖而非WSD使CD + 果糖组的厚壁菌门：拟杆菌门比值增加88%，WSD + 果糖组增加63%。WSD小鼠中的 丰度比CD小鼠高63倍，WSD + 果糖小鼠中的 丰度比CD + 果糖小鼠高330倍。食用WSD或高果糖摄入对肠道通透性和微生物群有不同影响。这些差异是否与不同的临床结果相关，即WSD主要促进体重增加，高果糖摄入导致屏障功能障碍，需要在未来的研究中进行调查。
