Abstract
Hypothalamic-pituitary-gonadal (HPG) axis activation occurs three times in life: the first is during fetal life, and has a crucial role in sex determination, the second time is during the first postnatal months of life, and the third is with the onset of puberty. These windows of activation recall the three windows of the “Developmental Origin of Health and Disease” (DOHaD) paradigm and may play a substantial role in several aspects of human development, such as growth, behavior, and neurodevelopment. From the second trimester of pregnancy there is a peak in gonadotropin levels, followed by a decrease toward term and complete suppression at birth. This is due to the negative feedback of placental estrogens. Studies have shown that in this prenatal HPG axis activation, gonadotropin levels display a sex-related pattern which plays a crucial role in sex differentiation of internal and external genitalia. Soon after birth, there is a new increase in LH, FSH, and sex hormone concentrations, both in males and females, due to HPG re-activation. This postnatal activation is known as “minipuberty.” The HPG axis activity in infancy demonstrates a pulsatile pattern with hormone levels similar to those of true puberty. We review the studies on the changes of these hormones in infancy and their influence on several aspects of future development, from linear growth to fertility and neurobehavior.
Highlights
During embryogenesis, the pituitary gland begins synthesizing both Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH) at around 9 weeks of gestation [1]
The placenta produces Estrogens (E) and Progesterone (P), that rise during the third trimester. This has a negative effect on gonadotropin levels and results in a drop in LH and FSH in cord blood at birth in healthy infants of both sexes [6,7,8]
The aim of this review is to summarize the current understanding on minipuberty and its role as a temporary window of opportunity for diagnosis and possible treatment in babies with disorders of sex development (DSD)
Summary
The pituitary gland begins synthesizing both Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH) at around 9 weeks of gestation [1]. LH and FSH can be detected in fetal blood from 12 to 14 weeks [2, 3] and start to be GnRH-dependent after 31–32 weeks [4, 5]. The structure of hCG is an analog of LH and may bind to the LH receptor, with similar biological effects on gonadal tissues [2, 6]. The placenta produces Estrogens (E) and Progesterone (P), that rise during the third trimester. This has a negative effect on gonadotropin levels and results in a drop in LH and FSH in cord blood at birth in healthy infants of both sexes [6,7,8]
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