Endocrine Abstracts

JOINT187

Introduction: Growth hormone (GH) therapy not only accelerates growth but also improves body composition of children with GH deficiency (GHD) by modulating lipid and carbohydrate metabolism. This effect is potentially mediated through adipokines secreted by adipose tissue and ghrelin. Additionally, maintaining proper phosphate balance is crucial for linear growth. Fibroblast growth factor 23 (FGF23), a key regulator of phosphorus levels in the blood, may contribute to the increased renal phosphorus reabsorption observed during recombinant human GH (rhGH) therapy. This study explored the effects of one year of rhGH therapy on body composition, adipokines, acylated/unacylated ghrelin (AG/UAG), and FGF23 in children with GHD.

Materials and Methods: This prospective observational study of 42 prepubertal, non-obese children with GHD undergoing their first year of rhGH replacement therapy. Changes in body composition, adipokine levels, AG/UAG, and FGF23 were evaluated at baseline and compared to results after 6 and 12 months of treatment.

Results: The participants, with an average age of 9. 2±2. 6 years, experienced significant growth acceleration. Over the 12-month period, total body fat decreased markedly, the lipid profile improved, and bone mineral density (BMD) showed a significant increase. Leptin and UAG levels dropped substantially, while adiponectin and AG concentrations increased. Plasma cFGF23 and IGF1 levels rose significantly, correlating with higher serum phosphate levels. However, FGF23 concentration changes did not affect BMD. The observed correlation between FGF23, IGF1, and height SDS suggests a potential role of FGF23 in linear growth. Regression analysis indicated that rhGH therapy influenced leptin and adiponectin levels independently of lean or fat mass but had no direct impact on ghrelin.

Conclusions: GH replacement therapy improves body composition and modifies adipokine profiles in GHD children. It also directly affects leptin and adiponectin levels regardless of body composition. Additionally, GHD children show increased serum phosphate levels, which appear linked to an upregulation of FGF23 rather than suppression, challenging the conventional understanding of FGF23’s phosphaturic role. Further studies are necessary to uncover the molecular pathways through which the GH/IGF1 axis regulates adipokine secretion and alters FGF23 plasma levels.

Keywords GH deficiency, adipokines, ghrelin, IGF1, body composition, FGF23.