Emerging evidence supports genetic determinants of FLD (eg PNPLA3, TM6SF2, MBOAT7, GCKR, HSD17B13) as determinants of insulin resistance and T2D. When dealing with FLD as a potential risk factor for T2D, it is straightforward to think of hepatic insulin resistance as the most relevant underlying mechanism. Conversely, a direct and independent contribution of FLD per se on risk of developing T2D is still a controversial topic. A consensus of experts has recently proposed the novel definition of ‘metabolic dysfunction‐associated fatty liver disease, MAFLD’ instead of ‘nonalcoholic fatty liver disease, NAFLD’, emphasizing the central role of dysmetabolism in the disease pathogenesis. The causal role of abdominal overweight/obesity, insulin resistance and type 2 diabetes (T2D) on the risk of fatty liver disease (FLD) has robustly been proven. Our meta-analyses demonstrated that GCKR rs780094 variant confers high cross-ethnicity risk for the development of T2DM, while significant associations between GCK, MTNR1B and G6PC2 variants and T2DM risk are limited to Caucasians. We also examined the studies for heterogeneity, as well as for bias of the publications.Ī total of 113,025 T2DM patients and 199,997 controls from 38 articles were included in the meta-analysis. Using the data from the retrieved articles, we computed summary estimates of the associations of the four variants with T2DM risk. We therefore performed a meta-analysis to derive a more precise estimation of the association between these polymorphisms and T2DM.Īll the publications examining the associations of these variants with risk of T2DM were retrieved from the MEDLINE and EMBASE databases. The evidence that the variants GCK rs1799884, GCKR rs780094, MTNR1B rs10830963 and G6PC2 rs560887, which are related to fasting plasma glucose levels, increase the risk of type 2 diabetes mellitus (T2DM) is contradictory.
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