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Erschienen in: Inflammation Research 4/2019

23.02.2019 | Original Research Paper

The influence of ICAM1 rs5498 on diabetes mellitus risk: evidence from a meta-analysis

verfasst von: Wensheng Mi, Yan Xia, Yanhui Bian

Erschienen in: Inflammation Research | Ausgabe 4/2019

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Abstract

Objectives

Both type 1 diabetes (T1D) and type 2 diabetes (T2D) are classified as forms of diabetes mellitus (DM) and commonly considered inflammatory process. Intercellular adhesion molecule-1 (ICAM-1) is involved in the development and progression of diabetes mellitus. However, the genetic association between ICAM-1 rs5498, and T1D and T2D risk was inconclusive.

Materials and methods

A meta-analysis by searching the PubMed, Embase, Cochrane Library, and Chinese National Knowledge Infrastructure (CNKI) databases was performed out. The pooled odds ratio (OR) and 95% confidence interval (CI) were used to describe the strength of association of T1D and T2D risk.

Results

A total of 14 studies encompassing 3233 cases and 2884 controls were included in the present meta-analysis. Significant associations were found between the allele and recessive models of ICAM1 rs5498 and DM in Asian population (allele: OR 1.13; 95% CI 1.03–1.23, p = 0.008; recessive: OR 1.25; 95% CI 1.06–1.48, p = 0.008), but not in Caucasian population (p > 0.05). In addition, the allele model of rs5498 was found to be significantly associated with the increased risk of T2D (OR 1.10; 95% CI 1.01–1.21, p = 0.03), but not T1D (p > 0.05).

Conclusions

The ICAM1 rs5498 might be a susceptible factor for T2D, but not T1D. And the allele and recessive models of ICAM1 rs5498 might be a risk factor in Asian population.
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Metadaten
Titel
The influence of ICAM1 rs5498 on diabetes mellitus risk: evidence from a meta-analysis
verfasst von
Wensheng Mi
Yan Xia
Yanhui Bian
Publikationsdatum
23.02.2019
Verlag
Springer International Publishing
Erschienen in
Inflammation Research / Ausgabe 4/2019
Print ISSN: 1023-3830
Elektronische ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-019-01220-4

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