We aimed to describe the functional changes of Sertoli cells, based on the measurement of serum anti-Müllerian hormone (AMH) and inhibin B during treatment with GnRHa and after its withdrawal in boys with central precocious puberty. Six boys aged 0.8 to 5.5 yr were included. AMH was low at diagnosis in patients >1 yr but within the normal range in younger patients. AMH increased to normal prepubertal levels during treatment. After GnRHa withdrawal, AMH declined concomitantly with the rise in serum testosterone. At diagnosis, inhibin B was elevated and decreased throughout therapy, remaining in the upper normal prepubertal range. In patients with testicular volume above 4 mL AMH remained higher in spite of suppressed FSH. After treatment withdrawal, inhibin B rose towards normal pubertal levels. In conclusion, AMH did not decrease in patients <1 yr reflecting the lack of androgen receptor expression in Sertoli cells in early infancy. Serum inhibin B might result from the contribution of two sources: the mass of Sertoli cells and the stimulation exerted by FSH. Sertoli cell markers might provide additional tools for the diagnosis and treatment followup of boys with central precocious puberty.
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http://dx.doi.org/10.1155/2013/823064 | DOI Listing |
Animal Model Exp Med
January 2025
Guangdong Medical Laboratory Animal Center, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.
Background: Makorin ring finger protein 3 gene (MKRN3) gene mutation is the most common genetic cause of central precocious puberty (CPP) in children. Due to the lack of ideal MKRN3-modified animal model (MKRN3-modified mice enter puberty only 4-5 days earlier than normal mice), the related research is limited.
Methods: Therefore, the MKRN3-modified rabbit was developed using CRISPR (clustered regularly interspaced short palindromic repeats) gene editing technology.
J Pediatr Endocrinol Metab
January 2025
Department of Paediatrics, School of Medical Sciences, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Objectives: Kisspeptin plays a major role in the onset of puberty by stimulating the gonadotropin-releasing hormone (GnRH) neurons. The aim of this study was to investigate whether GnRH inhibits kisspeptin secretion via a negative feedback mechanism and potential associations between kisspeptin levels and other hormones of importance for pubertal onset.
Methods: Thirteen girls with suspected central precocious puberty underwent a GnRH stimulation test twice in a randomized, placebo-controlled manner.
J Pediatr Endocrinol Metab
January 2025
117977 The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.
Objectives: The gonadotropin-releasing hormone (GnRH) provocation test is crucial for diagnosing central precocious puberty (CPP). However, due to its invasion and high cost, it is essential to find a simpler biomarker. This study aimed to investigate the feasibility of fasting insulin (FINS) and insulin-like growth factor-1 (IGF-1) as potential biomarkers for diagnosing girls with CPP and to analyze their effects on puberty development.
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January 2025
Department of Pediatrics, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Objective: This study analyzed the changes in blood glucose and lipid metabolism levels in children with central precocious puberty (CPP) and the correlation between CPP and obesity.
Methods: In total, 88 children with CPP aged 6-10 years who were admitted to our hospital between January 2023 and June 2024 (the CPP group), and 88 children without CPP in the same age group who received health check-ups (the non-CPP group) were retrospectively enrolled in this study. General data [gender, age, bone age, and body mass index (BMI)] were collected.
J Endocr Soc
January 2025
Cellular and Molecular Endocrinology Laboratory LIM/25, Division of Endocrinology and Metabolism, Clinicas Hospital, School of Medicine, University of Sao Paulo, 01246-903 Sao Paulo, Brazil.
Human puberty is a dynamic biological process determined by the increase in the pulsatile secretion of GnRH triggered by distinct factors not fully understood. Current knowledge reveals fine tuning between an increase in stimulatory factors and a decrease in inhibitory factors, where genetic and epigenetic factors have been indicated as key players in the regulation of puberty onset by distinct lines of evidence. Central precocious puberty (CPP) results from the premature reactivation of pulsatile secretion of GnRH.
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