Abnormal proliferation of gut mycobiota contributes to the aggravation of Type 2 diabetes

Abstract

AbstractType 2 diabetes (T2D) constitutes a worldwide health threat, and the underlying mechanism for the development and progression of T2D is complex and multifactorial. During the last decade, gut commensal bacteria have been found to play a crucial role in the regulation of T2D and related metabolic disorders. However, as a considerable component in gut microbiome, the relationship between mycobiota and T2D and related metabolic disorders remains unclear. As a proof-of-concept, we observed that the ablation of the commensal fungi in mice can protect HFD (High fat diet) induced insulin resistance and related metabolic disorders. Both ITS2 (internal transcribed spacer 2) sequencing and culture-dependent analysis show the enrichment of Candida albicans in samples from individuals with T2D (Chinese Clinical Trial Registry, ChiCTR2100042049). Repopulation with C. albicans in HFD mice accelerated insulin resistance and related disorders. Mechanically, we found the β-glucan from C. albicans mirrored the deteriorating effect of C. albicans through the dectin-1 dependent pathway. Our current findings support that gut mycobiota play an important role in the progress of T2D and indicated the preventing of gut mycobiota is a promising strategy to alleviate insulin resistance and related metabolic dysfunctions.