Giampaoli Ottavia, Conta Giorgia, Calvani Riccardo, Miccheli Alfredo
Department of Chemistry, Sapienza University of Rome, Rome, Italy.
NMR-Based Metabolomics Laboratory (NMLab), Sapienza University of Rome, Rome, Italy.
Front Nutr. 2020 Dec 23;7:606171. doi: 10.3389/fnut.2020.606171. eCollection 2020.
The global toll of type 1 diabetes (T1D) has steadily increased over the last decades. It is now widely acknowledged that T1D pathophysiology is more complex than expected. Indeed, a multifaceted interplay between genetic, metabolic, inflammatory and environmental factors exists that leads to heterogeneous clinical manifestations across individuals. Children with phenotype and those affected by T1D share low abundance of bifidobacteria, low content of short-chain fatty acids, intestinal phosphatase alkaline and a high incidence of inflammatory bowel diseases. In this context, host-gut microbiota dyad may represent a relevant contributor to T1D development and progression due to its crucial role in shaping host immunity and susceptibility to autoimmune conditions. The FUT2 gene is responsible for the composition and functional properties of glycans in mucosal tissues and bodily secretions, including human milk. FUT2 polymorphisms may profoundly influence gut microbiota composition and host susceptibility to viral infections and chronic inflammatory disease. In this minireview, the possible interplay between mothers' phenotype, host FUT2 genetic background and gut microbiota composition will be discussed in perspective of the T1D onset. The study of FUT2-gut microbiota interaction may add a new piece on the puzzling T1D etiology and unveil novel targets of intervention to contrast T1D development and progression. Dietary interventions, including the intake of α-(1, 2)-fucosyl oligosaccharides in formula milk and the use of specific prebiotics and probiotics, could be hypothesized.
在过去几十年中，1型糖尿病（T1D）的全球负担稳步增加。现在人们普遍认识到，T1D的病理生理学比预期的更为复杂。事实上，遗传、代谢、炎症和环境因素之间存在多方面的相互作用，导致个体间临床表现各异。具有某种表型的儿童以及受T1D影响的儿童双歧杆菌丰度低、短链脂肪酸含量低、肠道碱性磷酸酶水平低且炎症性肠病发病率高。在这种情况下，宿主-肠道微生物群二元组可能是T1D发生和发展的一个相关因素，因为它在塑造宿主免疫力和自身免疫性疾病易感性方面起着关键作用。FUT2基因负责黏膜组织和包括人乳在内的身体分泌物中聚糖的组成和功能特性。FUT2多态性可能会深刻影响肠道微生物群组成以及宿主对病毒感染和慢性炎症性疾病的易感性。在这篇综述中，将从T1D发病的角度探讨母亲表型、宿主FUT2基因背景和肠道微生物群组成之间可能的相互作用。对FUT2-肠道微生物群相互作用的研究可能会为令人困惑的T1D病因学增添新的内容，并揭示对抗T1D发生和发展的新干预靶点。可以设想进行饮食干预，包括在配方奶中摄入α-(1, 2)-岩藻糖基寡糖以及使用特定的益生元和益生菌。
