Can the FUT2 Non-secretor Phenotype Associated With Gut Microbiota Increase the Children Susceptibility for Type 1 Diabetes? A Mini Review.

Can the FUT2 Non-secretor Phenotype Associated With Gut Microbiota Increase the Children Susceptibility for Type 1 Diabetes? A Mini Review.
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DOI:
10.3389/fnut.2020.606171
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发表时间:
2020
影响因子:
5
通讯作者:
Miccheli A
Miccheli A
中科院分区:
农林科学2区
文献类型:
--
作者:
Giampaoli O;Conta G;Calvani R;Miccheli A

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在过去的几十年里,全球1型糖尿病(T1 D)的死亡人数稳步增加。现在人们普遍认为,T1 D的病理生理学比预期的更复杂。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,导致个体之间的异质性临床表现。具有非分泌型表型的儿童和受T1 D影响的儿童共享低丰度的双歧杆菌,低含量的短链脂肪酸,肠碱性磷酸酶和高发病率的炎症性肠病。在这种情况下,宿主肠道微生物群二分体可能代表T1 D发展和进展的相关贡献者,因为它在塑造宿主免疫力和对自身免疫性疾病的易感性方面起着至关重要的作用。FUT 2基因负责粘膜组织和身体分泌物(包括人乳)中聚糖的组成和功能特性。FUT 2多态性可能会深刻影响肠道微生物群组成和宿主对病毒感染和慢性炎症性疾病的易感性。在这篇小综述中,将从T1 D发病的角度讨论母亲表型、宿主FUT 2遗传背景和肠道微生物群组成之间可能的相互作用。FUT 2-肠道微生物群相互作用的研究可能会为令人困惑的T1 D病因学增加新的内容,并揭示新的干预靶点,以对比T1 D的发展和进展。可以假设饮食干预,包括在配方奶中摄入α-(1,2)-岩藻糖基低聚糖和使用特定的益生元和益生菌。
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 non-secretor 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.
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