Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Feb 27;11(5):1303.
doi: 10.3390/jcm11051303.

IL-1β Implications in Type 1 Diabetes Mellitus Progression: Systematic Review and Meta-Analysis

Affiliations
Review

IL-1β Implications in Type 1 Diabetes Mellitus Progression: Systematic Review and Meta-Analysis

Fátima Cano-Cano et al. J Clin Med. .

Abstract

During Type 1 Diabetes Mellitus (T1DM) progression, there is chronic and low-grade inflammation that could be related to the evolution of the disease. We carried out a systematic review and meta-analysis to evaluate whether peripheral levels of pro-inflammatory markers such as interleukin-1 beta (IL-1β) is significantly different among patients with or without T1DM, in gender, management of the T1DM, detection in several biological fluids, study design, age range, and glycated hemoglobin. We searched PubMed, Embase, Web of Science, and Scopus databases, and 26 relevant studies (2186 with T1DM, 2047 controls) were included. We evaluated the studies’ quality using the Newcastle−Ottawa scale. Meta-analyses were conducted, and heterogeneity and publication bias were examined. Compared with controls, IL-1β determined by immunoassays (pooled standardized mean difference (SMD): 2.45, 95% CI = 1.73 to 3.17; p < 0.001) was significantly elevated in T1DM. The compared IL-1β levels in patients <18 years (SMD = 2.81, 95% CI = 1.88−3.74) was significantly elevated. The hemoglobin-glycated (Hbg) levels in patients <18 years were compared (Hbg > 7: SMD = 5.43, 95% CI = 3.31−7.56; p = 0.001). Compared with the study design, IL-1β evaluated by ELISA (pooled SMD = 3.29, 95% CI = 2.27 to 4.30, p < 0.001) was significantly elevated in T1DM patients. IL-1β remained significantly higher in patients with a worse management of T1DM and in the early stage of T1DM. IL-1β levels determine the inflammatory environment during T1DM.

Keywords: IL-1β; chronic inflammation; meta-analysis; systematic review; type 1 diabetes mellitus.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Flow diagram. Identification and selection process of relevant studies comparing IL-1β levels between T1DM patients and controls.
Figure 2
Figure 2
Forest plot graphically representing the meta-analyses evaluating the changes in circulating IL-1β levels between T1DM patients and controls (random-effects models, inverse-variance weighting based on the DerSimonian and Laird method). Standardized mean difference (SMD) was chosen as effect size measure. An SMD > 0 suggests that IL-1β levels are higher in T1DM. Diamonds indicate the overall pooled SMDs with their corresponding 95% confidence intervals (CI).
Figure 3
Figure 3
Canonical and contour funnel plots of the estimated circulating IL-1β levels (assessed across immunoassays) comparing type 1 diabetes mellitus and controls, expressed as standardized mean difference (SMD) against its standard error. The red vertical line corresponds to the pooled SMD estimated in the meta-analysis. The two diagonal intermittent lines represent their pseudo-95% CI. Contours represent the defined conventional levels of statistical significance (i.e., 0.01, 0.05, 0.10) accompanied by associated shaded regions. The black circles represent the 22 studies meta-analyzed.

Similar articles

Cited by

References

    1. Eizirik D.L., Colli M.L., Ortis F. The role of inflammation in insulitis and Β-cell loss in type 1 diabetes. Nat. Rev. Endocrinol. 2009;5:219–226. doi: 10.1038/nrendo.2009.21. - DOI - PubMed
    1. Vaarala O. Is the origin of type 1 diabetes in the gut? Immunol. Cell Biol. 2012;90:271–276. doi: 10.1038/icb.2011.115. - DOI - PubMed
    1. Uno S., Imagawa A., Okita K., Sayama K., Moriwaki M., Iwahashi H., Yamagata K., Tamura S., Matsuzawa Y., Hanafusa T., et al. Macrophages and dendritic cells infiltrating islets with or without beta cells produce tumour necrosis factor-α in patients with recent-onset type 1 diabetes. Diabetologia. 2007;50:596–601. doi: 10.1007/s00125-006-0569-9. - DOI - PubMed
    1. Donath M.Y., Dinarello C.A., Mandrup-Poulsen T. Targeting innate immune mediators in type 1 and type 2 diabetes. Nat. Rev. Immunol. 2019;19:734–746. doi: 10.1038/s41577-019-0213-9. - DOI - PubMed
    1. Pankewycz O.G., Guan J.-X., Benedict J.F. Cytokines as Mediators of Autoimmune Diabetes and Diabetic Complications. Endocr. Rev. 1995;16:164–176. doi: 10.1210/edrv-16-2-164. - DOI - PubMed