Résumé
Adolescent PCOS may have its origins in fetal life (intrauterine growth retardation, hyperandrogenism) or before puberty (through premature pubarche, obesity, early puberty). In the last few years, evidence has clearly emerged showing that peri-puberty is a high-risk period for PCOS development, through obesity and secondary insulin resistance, metabolic syndrome, and hyperandrogenism. PCOS is an obesity-related condition, with weight gain and obesity in adolescence contributing to its development. Moreover, it is well known that the risk of developing a binge eating disorder increases around pubertal onset and continues to rise through adolescence, leading to overweight and obesity. The association between childhood obesity and both insulin resistance and hyperinsulinemia has been well documented, especially in Tanner 1–3 girls. The concomitant elevation of insulin and testosterone suggests an interrelationship between these two hormones. The amount of abdominal fat is recognized as a major contributor to the severity of PCOS phenotypes, with increased abdominal adiposity exacerbating the endocrine, metabolic, and psychological features of PCOS. In addition to genetic factors, insulin resistance and hyperinsulinemia are involved in androgen biosynthesis by the ovary (in conjunction with LH), the development of metabolic syndrome, and the release of adipokines. Androgen excess is the cardinal feature of PCOS and causes a series of endocrine changes, including insulin resistance, hyperinsulinemia, metabolic syndrome, dyslipidemia, and increased LH secretion. PCOS is associated with increased GnRH and LH secretions. It has been reported that HA enhances the GnRH pulse frequency and the subsequently elevated LH secretion. Moreover, there are some data on the association of PCOS and EDCs in women. EDCs can modify neuroendocrine modulation, adipose tissue development, insulin secretion, and metabolic disorders, favoring PCOS development. Last, the role of gut microbiota was recently discussed in addition to the epigenetic regulation of neurotransmitters. Although PCOS can manifest at any age in reproductive life, it often develops during adolescence, coincident with pubertal activation of the hypothalamic-pituitary-ovarian axis, eating disorders, and obesity. Identifying peri-pubertal girls at risk of PCOS may prevent adulthood PCOS.