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article · Zagazig University Medical Journal

Study of Serum Fibroblast Growth Factor 23 and Its Relation to Insulin Resistance in Obese Patients

Abstract

Background: The prevalence of obesity has risen substantially in developing and western countries. Obesity presents a major problem leading to cardiometabolic consequences including insulin resistance (IR) and metabolic syndrome. Fibroblast growth factor 23 (FGF-23) plays a role in the metabolism and phosphate mineralization. The aim of the study was to investigate the relationship between IR, serum FGF23 alongside obesity in affected individuals. Methods: This is a case control study included 60 obese patients (BMI > 30 kg/m²) and 30 healthy controls. All participants underwent thorough history taking, clinical examination and laboratory investigations. Serum FGF-23 was measured, and IR was calculated using the Homeostatic Model Assessment of IR (HOMA-IR) in both groups. Results: Serum levels of FGF 23 were significantly elevated in obese patients (mean 46.97 ± 40.40 pg/ml) compared to controls (mean 40.97 ± 43.16 pg/ml) (p<0.001). Moreover, obese patients showed significantly higher HOMA-IR values than controls (P =0.009). Multivariate regression analysis revealed age (p=0.009), low-density lipoprotein (LDL) (p=0.002), and C-reactive protein (CRP) (p=0.042) as statistically significant parameters for obesity while gender (p=0.418) did not reach statistical significance. Conclusions: This study demonstrates that obese patients had significantly higher serum FGF23 levels and increased HOMA-IR values than non-obese. The multivariate analysis displayed age, LDL and CRP as predictors of obesity indicating their role in metabolic dysfunction associated with obesity. These findings suggest that FGF23 and IR play a part in obesity so further research of their mechanisms is necessary. Targeted interventions aimed at these factors may reduce health risks of obesity.

Research topics

  • Parathyroid Disorders and Treatments
  • Fibroblast Growth Factor Research
  • Metabolism, Diabetes, and Cancer

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DOI: 10.21608/zumj.2025.376277.3911

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