Needs Assessment and Description
Human puberty is triggered by the reemergence of gonadotropin-releasing hormone (GnRH) pulsatile secretion with progressive activation of the gonadal function. A number of factors have been identified in the complex regulatory neuroendocrine network that controls puberty initiation. KISS1 and KISS1R genes, which encode kisspeptin and its cognate receptor, respectively, are considered crucial factors for acquisition of normal reproductive function. Gain-of-function mutations of the KISS1 and KISS1R genes were recently implicated in the pathogenesis of GnRH-dependent or central precocious puberty, previously considered idiopathic. This live course for clinicians and reproductive scientists will examine these emerging factors.

Learning Objectives
At the conclusion of this session, participants should be able to:

1. Recognize the symptoms and signs of human central precocious puberty.
2. Identify the new factors implicated in the GnRH secretion.

ACGME Competency
Medical Knowledge

TEST QUESTION:

Which of the following best describes the mechanisms involved in central precocious puberty?

1. Precocious puberty has been classically defined as the onset of secondary sexual characteristics in girls younger than 9 years and in boys younger than 10½ years.
2. GnRH-dependent precocious puberty (GDPP), also known as central or true precocious puberty, refers to an early activation of the hypothalamic-pituitaryadrenal axis.
3. Children with precocious puberty typically present with premature sexual development with growth acceleration and progressive skeletal maturation that can result in premature epiphyseal closure and stature in untreated cases.
4. Central precocious puberty is much more frequent in boys than in girls.
5. Loss-of-function mutations of the KISS1R gene were described in patients with central precocious puberty.
6. Kisspeptin is a powerful inhibitor of the GnRH secretion, after binding to the G protein-coupled receptor KISS1R in the membrane of hypothalamic GnRH neurons.