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 study aimed to evaluate the association between circulating adipokines, pro-inflammatory cytokines, and glycemic management in children with type 1 diabetes mellitus (T1D).
A case-control study was carried out between April 12, 2025, and February 1, 2026, in pediatric and endocrine clinics in Thi-Qar. The research involved 150 subjects: 100 children diagnosed with TID and 50 healthy controls who were matched based on age and sex. Clinical and demographic details were recorded, and blood samples were obtained after fasting for biochemical testing. Glycemic markers, lipid levels, adipokines (adiponectin, leptin, resistin, visfatin), and inflammatory cytokines (TNF-α, IL-6, IL-1β, CRP) were evaluated using automated analyzers and ELISA methods in regulated laboratory settings.
The findings indicated that HbA1c levels were markedly higher in T1D patients versus controls (p<0.001), suggesting inadequate glycemic management. Children with diabetes exhibited significantly elevated fasting glucose levels and negative lipid profiles, characterized by increased cholesterol, triglycerides, and low-density lipoprotein cholesterol (LDL-C), alongside reduced high-density lipoprotein cholesterol (HDL-C). Furthermore, adiponectin levels were significantly reduced in the T1D group (p<0.001), whereas proinflammatory markers increased considerably, such as leptin (p<0.001) and TNF-α (p<0.001). These markers displayed notable positive correlations with HbA1c (P<0.001), signifying a strong link between systemic inflammation and glycemic dysregulation.
Type 1 diabetes in children is associated with an imbalance of adipokines and elevated pro-inflammatory cytokines, which correlate with poor glycemic control. Chronic elevated blood sugar may trigger inflammatory pathways and disrupt fat tissue, resulting in metabolic problems and immune system activation that exacerbate disease advancement.
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Copyright (c) 2026 Zahraa Al-Tameemi

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