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Inflammation Research

, Volume 68, Issue 4, pp 275–284 | Cite as

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

  • Wensheng Mi
  • Yan XiaEmail author
  • Yanhui Bian
Original Research Paper
  • 36 Downloads

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.

Keywords

Diabetes mellitus (DM) Intercellular adhesion molecule-1 (ICAM-1) Genetic association Meta-analysis 

Notes

Acknowledgements

This study was funded by the Youth Foundation of the Education Department of Hunan (17B035) and the construct program of the key discipline in Hunan province.

Compliance with ethical standards

Conflict of interest

The authors declare no conflict of interest.

Supplementary material

11_2019_1220_MOESM1_ESM.doc (47 kb)
Supplementary material 1 (DOC 47 KB)
11_2019_1220_MOESM2_ESM.doc (56 kb)
Supplementary material 2 (DOC 55 KB)
11_2019_1220_MOESM3_ESM.doc (39 kb)
Supplementary material 3 (DOC 39 KB)

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Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  1. 1.Department of Pathophysiology, School of Basic Medical ScienceChangsha Medical UniversityChangshaPeople’s Republic of China
  2. 2.Department of Human Anatomy, Histology and Embryology, Institute of NeuroscienceChangsha Medical UniversityChangshaPeople’s Republic of China

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