Association of Adipokines and Pro-Inflammatory Cytokines with Glycemic Control in Pediatric Type 1 Diabetes
DOI:
https://doi.org/10.58564/AIMCJ3.1.2026.258Keywords:
Type 1 diabetes; Adipokines; Pro-inflammatory cytokines; Glycemic control; Pediatric diabetes.Abstract
This research sought to assess the relationships among circulating adipokines, pro-inflammatory cytokines, and glycemic control in pediatric patients with type 1 diabetes mellitus (T1D).
A case-control analysis was conducted from April 12, 2025, to February 1, 2026, in pediatric and endocrine clinics in Thi-Qar. The study included 150 participants: 100 children with type 1 diabetes and 50 healthy controls matched by age and sex. Clinical and demographic information was documented, and fasting blood samples were gathered for biochemical analysis. Glycemic indicators, lipid profiles, adipokines (adiponectin, leptin, resistin, visfatin), and inflammatory cytokines (TNF-α, IL-6, IL-1β, CRP) were assessed using automated analyzers and ELISA techniques under controlled laboratory conditions.
Hemoglobin A1c (HbA1c) levels were significantly elevated in T1D patients compared to controls (p<0.001), indicating insufficient glycemic control. Children with diabetes showed notably higher fasting glucose levels and adverse lipid profiles, including elevated cholesterol, triglycerides, and low-density lipoprotein cholesterol (LDL-C), along with decreased high-density lipoprotein cholesterol (HDL-C). Additionally, adiponectin concentrations were markedly lower in the T1D group (p<0.001), while proinflammatory markers increased substantially, including leptin (p<0.001) and TNF-α (p<0.001). These markers showed significant positive correlations with HbA1c (P<0.001), indicating a robust association between systemic inflammation and glycemic dysregulation.
Pediatric type 1 diabetes is linked to an imbalance of adipokines and increased pro-inflammatory cytokines, which are associated with inadequate glycemic control. Persistent high blood sugar can activate inflammatory pathways and disrupt adipose tissue, leading to metabolic issues and immune system activation that worsen disease progression.
References
Downloads
Published
Issue
Section
License
Copyright (c) 2026 Zahraa Al-Tameemi

This work is licensed under a Creative Commons Attribution 4.0 International License.
The Al-Iraqia Medical College Journal uses a Creative Commons Attribution (4.0 international license) and its license of (CC Attribution 4.0.). This license allows the authors to hold ownership of the copyright of their articles. However, it allows users to download, print, and extract. Reuse, archive, and disseminate the article as long as the authors get the appropriate credit and the source of the work. The license also ensures that the published articles will be available as widely as possible and can be located in any scientific archives CC Attribution 4.0
