Home Medicine Serum α-Klotho and its association with testosterone in boys with central precocious puberty
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Serum α-Klotho and its association with testosterone in boys with central precocious puberty

  • Eu-seon Noh , Hye Young Jin and Il Tae Hwang EMAIL logo
Published/Copyright: November 11, 2025
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Journal of Pediatric Endocrinology and Metabolism
From the journal Journal of Pediatric Endocrinology and Metabolism Volume 39 Issue 1

Abstract

Objectives

α-Klotho is an anti-aging protein involved in insulin-like growth factor 1 (IGF-1) signaling and reproductive function. Studies in girls with central precocious puberty (CPP) reported elevated α-Klotho levels that declined with treatment, suggesting a potential biomarker role. Whether boys with CPP exhibit similar patterns remains unclear.

Methods

This study included 36 boys with CPP and 34 age-matched healthy controls. α-Klotho, gonadotropins, testosterone, IGF-1, and other biochemical parameters were measured at baseline. In 15 patients, measurements were repeated after 6 months of gonadotropin-releasing hormone (GnRH) agonist therapy.

Results

Boys with CPP showed advanced bone age, higher body mass index standard deviation score (SDS), and elevated luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and IGF-1 SDS compared with controls. Baseline α-Klotho levels did not differ. Serum α-Klotho correlated strongly with testosterone (r=0.755, p<0.001) and moderately with IGF-1 SDS (r=0.570, p<0.001), but not with gonadotropins. In multiple regression, testosterone (β=0.612, p=0.004) and IGF-1 SDS (β=0.317, p=0.033) were independent predictors of α-Klotho. After 6 months of GnRH agonist therapy, testosterone and gonadotropins decreased significantly, while α-Klotho showed a non-significant decline.

Conclusions

Unlike girls with CPP, boys did not show elevated or treatment-responsive α-Klotho levels. The correlation with testosterone suggests α-Klotho may reflect androgenic activity in boys rather than serve as a dynamic biomarker. These findings should be considered exploratory, and larger studies with longer follow-up are needed to clarify its role in puberty and potential sex-specific regulation.

Keywords: α-Klotho; central precocious puberty; testosterone; GnRH agonist

Introduction

Central precocious puberty (CPP) is characterised by the premature activation of the hypothalamic–pituitary–gonadal (HPG) axis [1], [2], [3]. Although less common in boys than in girls, CPP in boys requires careful evaluation due to its association with underlying central nervous system abnormalities and its potential impact on adult height and psychosocial development [4], [5], [6], [7].

α-Klotho is a transmembrane protein with endocrine functions, including the regulation of phosphate metabolism, insulin/insulin-like growth factor 1 (IGF-1) signalling, and possibly gonadal axis activity; its soluble form (s-Klotho) has been proposed as a biomarker for ageing and endocrine diseases [8], [9], [10], [11]. Recent studies, including our previous research in girls with CPP, have demonstrated elevated α-Klotho levels during precocious puberty that decline with gonadotropin-releasing hormone (GnRH) agonist treatment, suggesting its potential as both a diagnostic and treatment-monitoring biomarker [12].

However, whether similar α-Klotho dynamics occur in boys with CPP remains unclear. In adults, α-Klotho levels have been associated with testosterone concentrations [13], and experimental studies suggest that testosterone upregulates Klotho expression via androgen receptor pathways [14]. These findings raise the possibility that Klotho expression may be differentially regulated by sex steroids in a sex-specific manner during puberty.

Building upon our findings in girls with CPP, we conducted a comparable study in boys to investigate whether α-Klotho follows a similar pattern. Specifically, we examined the associations between α-Klotho levels, growth parameters, and sex hormone levels in boys with CPP, and evaluated changes in α-Klotho following GnRH agonist therapy, using age-matched healthy boys as controls. This study aimed to determine whether α-Klotho could serve as a responsive biomarker in boys with CPP and to explore potential sex differences in its endocrine regulation during puberty.

Materials and methods

Participants and study design

A prospective observational study was conducted, including 36 boys diagnosed with idiopathic CPP and 34 age-matched healthy prepubertal boys. All patients with CPP underwent brain MRI to exclude organic causes. Patients with known brain tumours, prior cranial irradiation, or abnormal findings suggestive of central nervous system lesions were excluded. Patients diagnosed with CPP were treated with subcutaneous leuprorelin acetate, administered every 4 weeks in the following doses: 1.875 mg (0.5 vial) for those weighing<20 kg, 2.81 mg (0.75 vial) for those weighing 20–30 kg, and 3.75 mg (1 vial) for those weighing ≥30 kg. Medical records were collected for both groups, including data from before CPP diagnosis and 6 months after the initiation of GnRH agonist treatment. This study was approved by the Institutional Review Board of Hallym University Kangdong Sacred Heart Hospital (Institutional Review Board No. 2023-08-015).

Definition of CPP

The criteria for diagnosing CPP in this study required the onset of testicular enlargement (≥4 mL) before the age of 9 years, with confirmatory testing performed before the age of 10 years, including bone age advanced by at least 1 year compared to chronological age and a peak luteinizing hormone (LH) concentration ≥5 IU/L during the GnRH stimulation test.

Biochemical measurements

The following laboratory parameters were measured in the study participants: LH, follicle-stimulating hormone (FSH), testosterone, IGF-1, alkaline phosphatase (ALP), calcium, phosphate, and α-Klotho. Serum α-Klotho levels were quantified using an α-Klotho enzyme-linked immunosorbent assay kit (Immuno-Biological Laboratories Co., Japan). The measurement range was 93.75–6,000 pg/mL with a sensitivity of 6.15 pg/mL. The intra- and inter-assay coefficients of variation were 2.9–3.1 % and 2.9–11.4 %, respectively.

Statistical analysis

Statistical analyses were performed using SPSS version 21.0. To compare continuous variables between groups (control, before treatment, and 6 months after GnRH agonist treatment), independent-samples and paired-samples t-tests were used as appropriate. Partial correlation analysis was conducted to examine the associations between α-Klotho levels and hormonal parameters (testosterone, IGF-1, LH, and FSH), while controlling for potential confounders such as age and BMI SDS. In addition, multiple regression analyses were performed to identify independent predictors of α-Klotho, including testosterone, IGF-1 SDS, age, BMI SDS, LH, and FSH as covariates.

Results

Baseline characteristics: comparison between CPP boys and controls

Compared with age-matched prepubertal boys (controls), boys with CPP had significantly more advanced bone age (11.36±0.80 vs. 9.57±1.50 years, p<0.001) and a higher body mass index (BMI) standard deviation score (SDS) (0.87±1.22 vs. −0.21±0.82, p<0.001). Basal LH and FSH levels were significantly elevated in boys with CPP (LH: 1.18±0.63 vs. 0.12±0.05 mIU/mL, p<0.001; FSH: 3.39±2.38 vs. 1.79±1.09 mIU/mL, p=0.014), as were testosterone levels (0.39±0.60 vs. 0.10±0.04 ng/mL, p=0.034). IGF-1 SDS was also significantly higher in the CPP group (−0.19±0.74 vs. −0.99±0.32, p<0.001), reflecting activation of the GH-IGF-1 axis. ALP levels were modestly increased (288.62±66.30 vs. 254.23±46.39 IU/L, p=0.008). No significant differences were observed in serum calcium, phosphate, or α-Klotho concentrations between the two groups (α-Klotho: 2,080±1,159 vs. 1,888±933.2 pg/mL, p=0.45) (Table 1).

Table 1:

Baseline characteristics: boys with CPP vs. controls.

Control (prepubertal)

n=34		 CPP

n=36		 p-Value
Age, years 9.54±0.79 9.68±0.28 NS
Bone age, years 9.57±1.50 11.36±0.80 <0.001
BMI SDS −0.21±0.82 0.87±1.22 <0.001
Basal LH, mIU/mL 0.12±0.05 1.18±0.63 <0.001
Basal FSH, mIU/mL 1.79±1.09 3.39±2.38 0.014
Peak LH, mIU/mL Not done 16.02±9.32 Not comparable
Peak FSH, mIU/mL Not done 9.93±5.87 Not comparable
Testosterone, ng/mL 0.10±0.04 0.39±0.60 0.034
Calcium, mg/dL 9.85±0.26 9.92±0.30 NS
Phosphate, mg/dL 4.76±0.52 4.80±0.45 NS
ALP, IU/L 254.23±46.39 288.62±66.30 0.008
IGF-I SDS −0.99±0.32 −0.19±0.74 <0.001
α-Klotho, pg/mL 2,080±1,159 1,888±933.2 NS

  1. BMI, body mass index; CPP, central precocious puberty; n, number; NS, not significant; SDS, standard deviation score.

Change after GnRH agonist treatment

In the subset of 15 boys with CPP followed longitudinally, pubertal suppression with GnRH agonist treatment resulted in a significant deceleration of skeletal maturation, as evidenced by a reduced rate of bone age progression (mean bone age increased modestly from 11.33±0.88 to 11.79±0.79 years, p=0.002). Basal and peak LH and FSH levels were markedly suppressed (all p≤0.005), and testosterone levels declined from 0.45±0.75 to 0.11±0.03 ng/mL, although this change did not reach statistical significance (p>0.05). No significant changes were observed in BMI SDS, calcium, phosphate, ALP, or IGF-1 SDS over the 6-month period. Serum α-Klotho levels decreased slightly after treatment (from 2,292±909.8 to 2,214±715.5 pg/mL), but this change was not statistically significant (p=0.584) (Table 2).

Table 2:

Clinical, hormonal, and metabolic parameters of boys with CPP at diagnosis and after 6 months of GnRH agonist therapy.

Before treatment

n=15		 6 months after treatment

n=15		 p-Value
Age, years 9.69±0.27 10.19±0.27 NS
Bone age, years 11.33±0.88 11.79±0.79 0.002
BMI SDS 1.23±1.40 1.22±1.25 NS
Basal LH, mIU/mL 0.86±0.81 0.13±0.11 0.002
Basal FSH, mIU/mL 3.22±1.92 0.41±0.12 <0.001
Peak LH, mIU/mL 15.67±7.122 1.54±1.04 0.005
Peak FSH, mIU/mL 8.63±3.76 0.67±0.20 <0.001
Testosterone, ng/mL 0.45±0.75 0.11±0.03 NS
Calcium, mg/dL 9.96±0.32 9.97±0.33 NS
Phosphate, mg/dL 4.95±0.52 4.99±0.82 NS
ALP, IU/L 312.71±71.94 278.28±40.42 NS
IGF-I SDS 0.28±1.09 −0.04±0.97 NS
α-Klotho, pg/mL 2,292±909.8 2,214±715.5 NS

  1. BMI, body mass index; CPP, central precocious puberty; n, number; NS, not significant; SDS, standard deviation score.

Correlation analysis

Partial correlation analysis, adjusted for age and BMI SDS, revealed a strong positive correlation between α-Klotho and serum testosterone levels (r=0.755, p<0.001). α-Klotho was also positively correlated with IGF-1 SDS (r=0.570, p<0.001). No significant correlations were observed between α-Klotho and gonadotropins (LH: r=0.070, p=0.675; FSH: r = −0.017, p=0.919) (Table 3).

Table 3:

α-Klotho relationship with LH, FSH, estradiol, and IGF-I SDS studied by partial correlation with adjustment for age and BMI SDS.

Total
R p-Value
Basal LH 0.070 0.675
Basal FSH −0.017 0.919
Testosterone 0.755 <0.001
IGF-1 SDS 0.570 <0.001

  1. R, correlation coefficient; p, probability value; SDS, standard deviation score.

Regression analysis

In multiple regression analyses, the initial model including testosterone, IGF-1 SDS, age, and BMI SDS showed no independent predictors of α-Klotho, although IGF-1 SDS showed a trend toward positive association. In the extended model including gonadotropins, testosterone (β=0.612, p=0.004), IGF-1 SDS (β=0.317, p=0.033), and LH (β = −0.613, p=0.009) emerged as significant independent predictors of α-Klotho, while FSH was not significant (Table 4).

Table 4:

Multiple regression analyses for predictors of α-Klotho in boys with CPP and controls.

Model 1 independent variables β (standardized) p-Value
Testosterone 0.207 0.163
IGF-1 SDS 0.233 0.121
Age −0.182 0.169
BMI SDS −0.144 0.278
Overall model R2=0.201 Adj R2=0.135 p=0.027
Model 2 independent variables β (standardized) p-Value
Testosterone 0.612 0.004
IGF-1 SDS 0.317 0.033
Age −0.156 0.215
BMI SDS −0.254 0.059
LH −0.613 0.009
FSH 0.753 0.455
Overall model R2=0.319 Adj R2=0.231 p=0.005

  1. β, standardized regression coefficient; SDS, standard deviation score; R2, coefficient of determination; Adj R2, adjusted coefficient of determination.

Discussion

This study examined the role of α-Klotho in boys with CPP and highlights potential sex-specific differences compared with girls. While previous reports in girls demonstrated elevated and treatment-sensitive α-Klotho levels [12], our study did not observe such changes in boys. This sex difference may suggest that α-Klotho regulation during puberty differs between males and females.

Instead, we observed a correlation between testosterone and α-Klotho in boys. Previous population-based and experimental studies have demonstrated that testosterone positively regulates Klotho expression via androgen receptor-mediated pathways [13], and our findings appear consistent with this mechanism. In addition, exploratory multiple regression analyses indicated that testosterone and IGF-1 SDS were independent predictors of α-Klotho. LH also showed a statistically significant association, but in a negative direction, which is biologically less plausible and may reflect instability due to the small sample size. Therefore, these findings should be regarded as preliminary and interpreted with caution.

Another relevant finding is the moderate but significant correlation between α-Klotho and IGF-1. α-Klotho interacts with the insulin/IGF-1 signalling axis [10], and prior studies have linked its expression to growth factor status and bone metabolism. Our findings are broadly consistent with reports in healthy children and obese populations, where IGF-1 and α-Klotho levels vary together in relation to metabolic health [15], [16], [17].

Taken together, these preliminary findings raise the possibility that α-Klotho may have sex-specific roles during puberty. In girls, it has been suggested to act as a treatment-responsive marker of HPG axis activation, whereas in boys, it may be more reflective of androgenic milieu rather than a direct response to gonadotropin suppression. Given the small sample size and short follow-up, these interpretations should be considered exploratory, and further large-scale studies are needed to clarify these relationships.

This study has some limitations, including a relatively small sample size, a single-centre design, and a follow-up duration limited to 6 months. This short follow-up may have reduced our ability to detect longer-term changes in α-Klotho levels, and future studies with extended follow-up are warranted, ideally with larger sample sizes to confirm and expand our findings. Despite these limitations, the findings provide preliminary insights into sex-specific endocrine regulation and highlight the potential of α-Klotho as a biological marker of androgenic status in boys.

Conclusions

In boys with CPP, baseline α-Klotho levels did not appear to be markedly elevated and showed no clear changes after 6 months of GnRH agonist therapy. The observed correlation with testosterone raises the possibility that α-Klotho may reflect certain aspects of androgenic activity, although these findings should be considered exploratory given the small sample size. Larger studies with longer follow-up are needed to clarify its role in pubertal development and to further explore potential sex-specific regulatory mechanisms.

Corresponding author: Il Tae Hwang, Department of Pediatrics, Kangdong Sacred Heart Hospital, Seoul, Republic of Korea, E-mail:

Funding source: Kangdong Sacred Heart Hospital, Hallym University

Award Identifier / Grant number: 2024-06

Acknowledgments

Supported by a grant no. 2024-06 from the Kangdong Sacred Heart Hospital.

  1. Research ethics: This study was approved by the Institutional Review Board of Hallym University Kangdong Sacred Heart Hospital (Institutional Review Board No. 2023-08-015) and conducted in accordance with the Declaration of Helsinki (as revised in 2013).

  2. Informed consent: Informed consent was obtained from all individuals included in this study, or their legal guardians or wards.

  3. Author contributions: All authors have accepted responsibility for the entire content of this manuscript and approved its submission.

  4. Use of Large Language Models, AI and Machine Learning Tools: None declared.

  5. Conflict of interest: The authors state no conflict of interest.

  6. Research funding: Supported by a grant no. 2024-06 from the Kangdong Sacred Heart Hospital.

  7. Data availability: The datasets generated and/or analyzed during the current study are available from the corresponding author upon reasonable request.

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Received: 2025-08-12
Accepted: 2025-10-23
Published Online: 2025-11-11
Published in Print: 2026-01-23

© 2025 the author(s), published by De Gruyter, Berlin/Boston

This work is licensed under the Creative Commons Attribution 4.0 International License.

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https://doi.org/10.1515/jpem-2025-0456
Keywords for this article
α-Klotho; central precocious puberty; testosterone; GnRH agonist
Creative Commons
BY 4.0

Articles in the same Issue

  1. Frontmatter
  2. Review
  3. Prevalence of congenital hypothyroidism in infants of mothers with hypothyroidism: a meta-analysis
  4. Original Articles
  5. Pubertal characteristics, final height, and associated factors in patients with nonclassical congenital adrenal hyperplasia: a single center experience
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  7. Bioelectrical impedance analysis and hormonal assessment in adolescents with pubertal gynecomastia
  8. The relationship between FSTL-1 (follistatin-related protein 1), FAM19A5 (family with sequence similarity 19, member A5) and CTRP-6 (C1q/TNF-related protein 6) levels and metabolic parameters in overweight children
  9. Role of hyperandrogenism on disordered eating behaviors in adolescents with PCOS and interplay with insulin resistance
  10. The impact of hepatic steatosis on epicardial adipose tissue in obese individuals
  11. Exploratory real-world experience with GLP-1 receptor agonists vs. metformin in youth with new-onset type 2 diabetes: a single-center retrospective study
  12. Characterization of monogenic diabetes among Sudanese children: a multi-center experience from a population with high consanguinity
  13. Short Communication
  14. Implementation and feasibility of a nutrition assessment for recently diagnosed youth with type 2 diabetes
  15. Case Reports
  16. Noonan syndrome and autoimmune hepatitis: patient report and literature review
  17. Adrenal oncocytoma: an unusual etiology of Cushing’s syndrome in an adolescent female
  18. Novel MCT8 mutation: diagnostic value of T3/T4 ratio
  19. Clinical insights of the TBX19 C.856 C>T variant: a case report and literature review on neonatal isolated ACTH deficiency
  20. Wolcott–Rallison syndrome due to a novel homozygous missense variation (p.Gly602Val) in the exon 11 of EIF2AK3 gene
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