Background
Some genetic association studies tried to investigate potential associations of Transcription Factor 7 Like 2 (
TCF7L2
) rs7903146 polymorphism with type 2 diabetes mellitus (T2DM). However, the results of these studies were not consistent. Thus, we performed the present meta-analysis to explore associations between
TCF7L2
rs7903146 polymorphism and T2DM in a larger pooled population.
Methods
Systematic literature research of PubMed, Web of Science and Embase was performed to identify eligible studies for pooled analyses. I
2
statistics were employed to assess between-study heterogeneities. If I
2
was greater than 50%, random-effect models (REMs) would be used to pool the data. Otherwise, fixed-effect models (FEMs) would be applied for synthetic analyses.
Results
Totally 68 studies with 115,809 subjects were included for analyses. The pooled analyses showed that
TCF7L2
rs7903146 (dominant model:
p
< 0.0001; recessive model:
p
< 0.0001; over-dominant model:
p
< 0.0001; allele model:
p
< 0.0001) polymorphism was significantly associated with susceptibility to T2DM in overall population. Further subgroup analyses revealed similar significant findings in both Asians and Caucasians.
Conclusions
In conclusion, our findings supported that
TCF7L2
rs7903146 polymorphism could be used to identify individuals at high risk of developing T2DM in Asians and Caucasians.
Electronic supplementary material
The online version of this article (10.1186/s13098-019-0451-9) contains supplementary material, which is available to authorized users.
Background: MiR-145 is involved in insulin resistance (IR) in liver cells, but its effects in human umbilical vein endothelial cells (HUVECs) induced by IR remains unclear. This study took this as the starting point, aiming to find a potential target for the treatment of related disease.
Methods: HUVECs were respectively treated with glucose of 15, 30, 45 mmol/L, or insulin of 1, 2, 3, 4, 5 μmol/L on the basis of high-glucose (33.3 mmol/L). MiR-145 mimics and miR-145 inhibitor were severally transfected into HUVECs with or without IR (4 μmol/L insulin + high-glucose). Quantitative real-time polymerase chain reaction (qRT-PCR) assay determined the miR-145 expression in HUVECs after treatment and transfection. The glucose consumption and glycogen contents of cells were appraised by glucose oxidase-peroxidase and anthranone-sulfuric acid methods, respectively. The apoptotic rates were ascertained using the flow cytometry. The expressions of apoptosis-related indicators Bcl-2 and Bax were analyzed by western blot (WB) and qRT-PCR assays.
Results: The expression of miR-145 was increased in IR models and incremental glucose concentrations. The glucose consumption and glycogen content were down-regulated in IR-induced HUVECs, which were enhanced by over-expressed miR-145 but reversed by down-regulation. Moreover, over-expression of miR-145 aggravated the apoptosis of IR-induced HUVECs, while the inhibition of miR-145 had a completely opposite effect. Accordingly, up-regulated miR-145 obviously reduced Bcl-2 level and enhanced Bax expression in IR models, which was contrary to the down-regulated miR-145.
Conclusion: Down-regulated miR-145 rescued IR in endothelial cells, which might be a conceivable treatment for IR of endothelial cells.
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