The pathophysiological role of Adiponectin, Insulin Growth Factor-1 (IGF-1) and Growth Factor Binding Protien-3 (IGFBP-3) in thyrotoxicosis patients

Abstract

Background: Adiponectin, insulin-like growth factor-1 (IGF-1), and insulin-like growth factor-binding protein-3 (IGFBP-3) play vital roles in endocrine regulation, energy homeostasis, growth, and metabolism, and have been shown to interfere with thyroid hormones.
Aim: This study seeks to detect the pathophysiological roles of adiponectin, IGF-1, and IGFBP-3 and to assess their relationships with thyroid hormone levels in patients with thyrotoxicosis.
Material and Methods: A case-control study was conducted, involving 56 patients diagnosed with thyrotoxicosis and 30 healthy controls matched for age and gender. Serum levels of triiodothyronine (T3), thyroxine (T4), and thyroid-stimulating hormone (TSH) were measured by an automated chemiluminescence immunoassay (CLIA) system, and adiponectin, IGF-1, and IGFBP-3 were measured using human enzyme-linked immunosorbent assay (ELISA) kits.
Results: Patients with thyrotoxicosis exhibited significantly higher serum T3 and T4 levels and significantly lower TSH levels compared with healthy controls (p<0.0001). Serum adiponectin, IGF-1, and IGFBP-3 concentrations were significantly elevated in the patient group (p=0.004, p<0.0001, and p<0.0001, respectively). Patients with a positive family history demonstrated significantly higher adiponectin and IGF-1 levels, whereas IGFBP-3 levels were significantly higher among those without a family history. Correlation analysis revealed significant positive correlations between serum adiponectin and T3 (r=0.229, p=0.032) and T4 (r=0.240, p=0.049). while other correlations among the studied biomarkers were weak and non-significant.
Conclusions: Thyrotoxicosis is associated with significant increases in serum adiponectin, IGF-1, and IGFBP-3 levels, suggesting that these biomarkers may contribute to the metabolic and endocrine adaptations associated with excess thyroid hormone. Family history appears to influence adiponectin and IGF-1 concentrations, highlighting a potential genetic contribution to metabolic alterations in thyrotoxicosis. These findings support a role for adiponectin, IGF-1, and IGFBP-3 in the pathophysiology of thyrotoxicosis and warrant further investigation into their clinical significance