Lambertz Jessica, Weiskirchen Sabine, Landert Silvano, Weiskirchen Ralf
Institute of Molecular Pathobiochemistry, Experimental Gene Therapy and Clinical Chemistry (IFMPEGKC), RWTH University Hospital Aachen, Aachen, Germany.
Culture Collection of Switzerland AG (CCOS), Wädenswil, Switzerland.
Front Immunol. 2017 Sep 19;8:1159. doi: 10.3389/fimmu.2017.01159. eCollection 2017.
Fructose is one of the key dietary catalysts in the development of non-alcoholic fatty liver disease (NAFLD). NAFLD comprises a complex disease spectrum, including steatosis (fatty liver), non-alcoholic steatohepatitis, hepatocyte injury, inflammation, and fibrosis. It is also the hepatic manifestation of the metabolic syndrome, which covers abdominal obesity, insulin resistance, dyslipidemia, glucose intolerance, or type 2 diabetes mellitus. Commensal bacteria modulate the host immune system, protect against exogenous pathogens, and are gatekeepers in intestinal barrier function and maturation. Dysbalanced intestinal microbiota composition influences a variety of NAFLD-associated clinical conditions. Conversely, nutritional supplementation with probiotics and preobiotics impacting composition of gut microbiota can improve the outcome of NAFLD. In crosstalk with the host immune system, the gut microbiota is able to modulate inflammation, insulin resistance, and intestinal permeability. Moreover, the composition of microbiota of an individual is a kind of fingerprint highly influenced by diet. In addition, not only the microbiota itself but also its metabolites influence the metabolism and host immune system. The gut microbiota can produce vitamins and a variety of nutrients including short-chain fatty acids. Holding a healthy balance of the microbiota is therefore highly important. In the present review, we discuss the impact of long-term intake of fructose on the composition of the intestinal microbiota and its biological consequences in regard to liver homeostasis and disease. In particular, we will refer about fructose-induced alterations of the tight junction proteins affecting the gut permeability, leading to the translocation of bacteria and bacterial endotoxins into the blood circulation.
果糖是导致非酒精性脂肪性肝病(NAFLD)的关键饮食催化剂之一。NAFLD包括一系列复杂的疾病,包括脂肪变性(脂肪肝)、非酒精性脂肪性肝炎、肝细胞损伤、炎症和纤维化。它也是代谢综合征的肝脏表现,代谢综合征包括腹型肥胖、胰岛素抵抗、血脂异常、葡萄糖耐量异常或2型糖尿病。共生细菌调节宿主免疫系统,抵御外源病原体,是肠道屏障功能和成熟的守门人。肠道微生物群组成失衡会影响多种与NAFLD相关的临床状况。相反,补充影响肠道微生物群组成的益生菌和益生元可以改善NAFLD的预后。在与宿主免疫系统的相互作用中,肠道微生物群能够调节炎症、胰岛素抵抗和肠道通透性。此外,个体的微生物群组成是一种受饮食影响很大的指纹。此外,不仅微生物群本身,其代谢产物也会影响新陈代谢和宿主免疫系统。肠道微生物群可以产生维生素和包括短链脂肪酸在内的多种营养物质。因此,保持微生物群的健康平衡非常重要。在本综述中,我们讨论了长期摄入果糖对肠道微生物群组成的影响及其对肝脏稳态和疾病的生物学后果。特别是,我们将提及果糖诱导的紧密连接蛋白改变,影响肠道通透性,导致细菌和细菌内毒素进入血液循环。