Impact of Vitamin D Replacement on the Vitamin D-Leptin-Prolidase Axis in Secondary Hyperparathyroidism
Hormone and Metabolic Research, cilt.58, sa.8, ss.311-317, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 58 Sayı: 8
- Basım Tarihi: 2026
- Doi Numarası: 10.1055/a-2897-4134
- Dergi Adı: Hormone and Metabolic Research
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, Chemical Abstracts Core, EMBASE, MEDLINE, Academic Search Ultimate (EBSCO)
- Sayfa Sayıları: ss.311-317
- Anahtar Kelimeler: vitamin D deficiency, secondary hyperparathyroidism, bone metabolism, prolidase, metabolic syndrome, leptin
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
Severe vitamin D deficiency commonly results in secondary hyperparathyroidism and increased bone turnover. Despite the well-established inverse relationship between vitamin D and parathyroid hormone, the impact of vitamin D repletion on collagen matrix remodeling and adipose-bone signaling remains unclear, and the combined response of prolidase and leptin has not been previously examined. This prospective observational study included 36 female patients with severe vitamin D deficiency and secondary hyperparathyroidism who received oral vitamin D supplementation (50,000 IU/wk) for 8 weeks. Serum 25-hy-droxyvitamin D, parathyroid hormone, alkaline phosphatase, prolidase activity, and leptin levels were assessed before and after treatment, and correlations among biochemical changes were analyzed. Vitamin D supplementation significantly increased serum 25-hydroxyvitamin D levels and reduced parathyroid hormone and alkaline phosphatase concentrations (all p< 0.001). Serum prolidase activity increased significantly (p= 0.027), whereas leptin levels showed a modest, non-significant decrease. Changes in prolidase activity were positively associated with baseline parathyroid hormone levels and inversely related to parathyroid hormone reduction. Post-treatment vitamin D levels demonstrated a modest positive correlation with leptin concentrations (r= 0.347 and p= 0.045), while no significant associations were observed between changes in vitamin D and prolidase or leptin levels. Vitamin D repletion in patients with severe vitamin D deficiency-related secondary hyperparathyroidism was associated with distinct biochemical responses, with early collagen matrix remodeling reflected by increased prolidase activity and subtler changes in adipose-bone signaling. These findings suggest temporally divergent pathways of skeletal recovery and support prolidase as a potential dynamic marker of early matrix adaptation.