Telomere length is not altered in girls with idiopathic central precocious puberty treated with a GnRH analog – leuprolide acetate

Abstract

Background

Idiopathic central precocious puberty (iCPP) presents a disproportionate advancement of bone age and maturation, as well as metabolic and endocrinological changes that may be related to effects on telomere biology.

Objective

To investigate the telomere length in iCPP girls treated with GnRHa.

Study design

Observational case-control study with 85 girls, including 45 iCPP treated with GnRHa and 40 controls. It was analyzed age, height, weight and body mass index (BMI), insulin, triglycerides, testosterone, insulin resistance by HOMA, and telomere length by real-time PCR. Statistical analyses were determined by Wilcoxon test and Spearman correlation was carried out.

Results

Weight, BMI, insulin level and HOMA index were higher in the iCPP than in the control group (p < .01); without difference between mean ages. The telomere length did not differ between iCPP and control group. However, a negative correlation was observed between the telomere length and age in iCPP (p = .0009) and control group (p = .014), and weight in the iCPP (p = .017).

Conclusions

We did not observe any difference in the telomere length in the iCPP and control group. Even though, some characteristics of the disease, such as increased weight and body fat, negatively influence the telomere biology.

摘要

背景:特发性中枢性性早熟(iCPP)表现出骨龄和性成熟的不协调的提前, 代谢和内分泌的变化也可能与端粒体生物学效应有关。目的:探讨经促性腺激素释放激素类似物治疗的特发性中枢性性早熟女孩的端粒体长度。研究设计:对85名女孩进行观察性病例对照研究, 包括45名接受GnRHa治疗的特发性中枢性性早熟女孩和40名对照病例。通过分析年龄、身高、体重、体重指数、胰岛素、甘油三酯、睾酮、稳态模型评估法的胰岛素抵抗、实时PCR检测端粒长度。统计分析由Wilcoxon检验确定, 并进行了Spearman相关分析。结果：特发性中枢性性早熟组的体重、体重指数、胰岛素水平和HOMA指数均高于对照组（p < .01）。中枢性性早熟和对照组的平均年龄没有差别。特发性中枢性性早熟组和对照组的端粒长度没有差异。在特发性中枢性性早熟组(p =.0009)和对照组(p= .014)的端粒长度和年龄呈负相关, 在特发性中枢性性早熟组的端粒体长度 (p=017)和体重也呈负相关。结论:我们观察到特发性中枢性性早熟组和对照组之间端粒体长度没有任何差异。尽管如此, 这种疾病的某些特征, 如体重和体脂的增加, 对端粒体生物学效应方面产生了负面影响。

Keywords:

• Idiopathic central precocious puberty
• telomere length
• GnRH analog
• leuprolide acetate
• obesity

Acknowledgments

The authors are extremely grateful to the subjects and their families for participating in this study. We also thank Cristiana C. Padovan, Océlia de Vasconcelos for blood collection, Maria Albina Valladas Verceze and Tatiana Marina Vieira Giorgenon for technical assistance; and Suleimy Mazin for performing the statistical analysis.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This study was supported by the Sao Paulo Research Foundation (FAPESP, Fundação de Amparo à Pesquisa do Estado de São Paulo) with the grant 2012/11566-2 (RMR) and fellowship 2012/11069-9 (CLMF), National Council for Scientific and Technological Development (CNPq, Conselho Nacional de Desenvolvimento Cientifico Tecnológico), Coordination for the Improvement of Higher Education Personnel (CAPES, Coordenação de Aperfeiçoamento de Pessoal de Nível Superior; Academic Excellence Program – PROEX and Graduate Support Program – PROAP) and by the National Institutes of Science and Technology (INCT, Institutos Nacionais de Ciência e Tecnologia)

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