Serum 25-hydroxyvitamin D levels and the risk of idiopathic central precocious puberty in girls.

INTRODUCTION: Prior studies have found inconsistent results regarding the relationship between vitamin D status and Idiopathic Central Precocious Puberty (ICPP). OBJECTIVE: To assess the role of serum 25-hydroxyvitamin D (25 [OH]D) levels in ICPP development. METHOD: The authors retrospectively collected data from 221 girls with ICPP and 144 healthy girls between January 2017 and December 2019. The participants' serum 25(OH)D levels were measured using an automatic chemiluminescence method, and the association between serum 25(OH)D levels and the risk of ICPP was assessed using multivariate logistic regression analysis. Odds Ratios (OR) with 95% Confidence Intervals (95% CI) were calculated as effect estimates. RESULTS: Serum 25(OH)D levels in the ICPP group were significantly lower than those in healthy controls (p < 0.001). Multivariate analysis indicated that girls with insufficient vitamin D levels (OR = 0.201; 95% CI 0.094-0.428; p < 0.001) and sufficient vitamin D levels (OR = 0.141; 95% CI 0.053-0.375; p < 0.001) both had a lower risk of ICPP than girls with vitamin D deficiency. Moreover, the authors found that the height (p = 0.014), weight (p = 0.014), breast stage (p = 0.010), mother's height (p < 0.001), and luteinizing hormone/follicle-stimulating hormone ratio (p = 0.010) in girls with ICPP could be associated with levels of vitamin D. CONCLUSION: This study found that a low serum 25(OH)D level is an independent risk factor for ICPP, and several characteristics of girls with ICPP could be affected by their vitamin D status.

Serum 25-hydroxyvitamin D levels and the risk of idiopathic central precocious puberty in girls

Abstract Introduction Prior studies have found inconsistent results regarding the relationship between vitamin D status and Idiopathic Central Precocious Puberty (ICPP). Objective To assess the role of serum 25-hydroxyvitamin D (25 [OH]D) levels in ICPP development. Method The authors retrospectively collected data from 221 girls with ICPP and 144 healthy girls between January 2017 and December 2019. The participants' serum 25(OH)D levels were measured using an automatic chemiluminescence method, and the association between serum 25(OH)D levels and the risk of ICPP was assessed using multivariate logistic regression analysis. Odds Ratios (OR) with 95% Confidence Intervals (95% CI) were calculated as effect estimates. Results Serum 25(OH)D levels in the ICPP group were significantly lower than those in healthy controls (p < 0.001). Multivariate analysis indicated that girls with insufficient vitamin D levels (OR = 0.201; 95% CI 0.094-0.428; p < 0.001) and sufficient vitamin D levels (OR = 0.141; 95% CI 0.053-0.375; p < 0.001) both had a lower risk of ICPP than girls with vitamin D deficiency. Moreover, the authors found that the height (p = 0.014), weight (p = 0.014), breast stage (p = 0.010), mother's height (p < 0.001), and luteinizing hormone/follicle-stimulating hormone ratio (p = 0.010) in girls with ICPP could be associated with levels of vitamin D. Conclusion This study found that a low serum 25(OH)D level is an independent risk factor for ICPP, and several characteristics of girls with ICPP could be affected by their vitamin D status.

KISS1/KISS1R mediates Sertoli cell apoptosis via the PI3K/AKT signalling pathway in a high­glucose environment.

In male patients with diabetes, reduced sperm motility and fertility are observed. KiSS­1 metastasis suppressor (KISS1)/KISS1 receptor (KISS1R) serves an important role in regulating adolescent sexual maturity and reproductive system development in mammals; however, the mechanism underlying KISS1/KISS1R in reproductive dysfunction in male patients with diabetes is not completely understood. The aim of the present study was to examine the role of KISS1/KISS1R in Sertoli cells. High glucose (HG)­induced mouse Sertoli cells were used to model diabetes in vitro. KISS1/KISS1R overexpression and knockdown were established in mouse Sertoli cells. Reverse transcription­quantitative PCR and western blotting were performed to measure the expression levels of KISS1/KISS1R and apoptosis­related proteins. Cell viability and apoptosis was assessed by performing Cell Counting Kit­8, TUNEL staining and flow cytometry assays, respectively. Western blotting was performed to assess the expression levels of PI3K/AKT signalling­related proteins. KISS1/KISS1R expression levels were downregulated in HG­induced mouse Sertoli cells compared with control cells. KISS1/KISS1R overexpression significantly suppressed HG­induced apoptosis and decrease of viability in mouse Sertoli cells. Moreover, the western blotting results indicated that KISS1/KISS1R activated PI3K/AKT signalling. Treatment with PI3K/AKT pathway inhibitor significantly reversed KISS1/KISS1R­mediated protective effects. Collectively, the results of the present study suggested that KISS1/KISS1R mediated Sertoli cell apoptosis via the PI3K/AKT signalling pathway under HG conditions, which provided reliable targets for the treatment of reproductive dysfunction in male patients with diabetes.