Abstract / Summary
Childhood overweight and obesity have been associated with earlier pubertal onset most commonly in girls than boys. This review aims to summarize proposed mechanisms involved in early puberty amongst children with increased weight and possibly help early detection and reduce any long-term related risks associated with precocious puberty in overweight and obese children. Adipose tissue functions as an endocrine organ and produces several signaling molecules that may influence puberty initiation. Among these, leptin appears to provide an important permissive signal linking energy availability with activation of the hypothalamic–pituitary–gonadal axis. Insulin and hyperinsulinemia may further influence pubertal timing through effects on hypothalamic kisspeptin signaling and ovarian and adrenal androgen production. Additional mechanisms involving sirtuin-mediated epigenetic regulation of Kiss1, the ghrelin–LEAP2 system, and the gut microbiota have also been proposed. Environmental endocrine-disrupting chemicals, including bisphenol A and phthalates, may provide additional links between adiposity and puberty. Clarifying these links is clinically important for monitoring pubertal progression and cardiometabolic risk in children with obesity, and for informing prevention and early intervention aimed at reducing long-term adverse outcome.