The Interplay Between Body Weight and the Onset of Puberty

This overview explores the complex relationship between environmental factors, particularly obesity, and the timing of puberty, with a focus on how hormonal and genetic interactions are influenced by external conditions. Puberty (Gonadarche) is characterized by the activation of the Hypothalamic - Pituitary - Gonadal (HPG) axis. The onset and progression of puberty vary significantly among individuals, primarily due to genetic factors, with key genes like KISS1 and MKRN3 playing a crucial role. Cohesively, this paper emphasizes that environmental factors, particularly obesity and exposure to endocrine-disrupting chemicals (EDCs) have become a significant facet affecting the timing of puberty. Childhood obesity has significantly risen in recent decades and the age of pubertal onset has declined over the same period. Obesity greatly disrupts hormone regulation in pre-pubertal children. Leptin accelerates the onset of puberty in girls but not in boys. The underlying mechanism is proposed to be the increase in Kiss1/GnRH signalling. On the contrary excess leptin in boys supresses the testosterone production by increasing oestrogen conversion. Low adiponectin in obese girls may contribute to earlier puberty due to reduced inhibition of the Kiss1/GnRH signalling. Low adiponectin in boys is linked to delayed puberty due to its role in maintaining insulin sensitivity and testosterone production. Hyperinsulinemia influences pubertal timing through central and peripheral mechanisms. Insulin acting synergistically with leptin promotes earlier onset of puberty in girls but not in boys. The effects of exposure to certain EDCs, mostly obesogenic that mimic the action of natural hormones on the timing of puberty is still unclear, hence the need for further research on this topic is required. Addressing and preventing obesity in children could potentially mitigate these alterations in pubertal timing.