Abstract
This study focuses on the latest developments in the studies of m6A modification and provides an up-to-date summary of the association between m6A modification and type 2 diabetes (T2D). The possible mechanisms of m6A related to T2D were summarized by literature review. The differentially expressed genes (DEGs) of m6A methylase in T2D were analyzed from 12 datasets in Gene Expression Omnibus (GEO). The associations between m6A level and T2D were explored in four electronic databases, including PubMed, EmBase, Web of Science and CNKI. Standard mean difference (SMD) and 95 % confidence interval (95 %CI) was calculated to assess the total effect in integrative analysis. Differential expression genes detected in at least three of six tissues were ZC3H13, YTHDC1/2, and IGF2BP2. LRPPRC were differentially expressed in five tissues except in arterial tissue. A total of 6 studies were included for integrative analysis. The mean m6A levels were significantly lower in T2D than those in normal controls (SMD = −1.35, 95 %CI: −2.58 to −0.11). This systematic review and integrative analysis summarize the previous studies on the association between m6A modification and T2D and the possible role of m6A modification in the progression of T2D, such as abnormal blood glucose, abnormal pancreatic β-cell function, insulin resistance, and abnormal lipid metabolism. The integrative analysis showed that decreased level of m6A was associated with T2D. These findings provide new targets for early detection and treatment for T2D.
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