title: Obesity and the pubertal transition in girls and boys.
abstract: Childhood obesity has become a major health concern in recent decades, especially with regard to metabolic abnormalities that impart a high risk for future cardiovascular disease. Recent data suggest that excess adiposity during childhood may influence pubertal development as well. In particular, excess adiposity during childhood may advance puberty in girls and delay puberty in boys. Obesity in peripubertal girls may also be associated with hyperandrogenemia and a high risk of adolescent polycystic ovary syndrome. How obesity may perturb various hormonal aspects of pubertal development remains unclear, but potential mechanisms are discussed herein. Insulin resistance and compensatory hyperinsulinemia may represent a common thread contributing to many of the pubertal changes reported to occur with childhood obesity. Our understanding of obesity's impact on pubertal development is in its infancy, and more research into pathophysiological mechanisms and longer-term sequelae is important.
authors.affiliation: Division of Endocrinology, Department of Pediatrics Center for Research in Reproduction Division of Endocrinology and Metabolism, Department of Medicine, University of Virginia Health System, PO Box 800391, Charlottesville, Virginia 22908, USA.
authors.forename: Christine M
authors.initials: CM
authors.lastname: Burt Solorzano
authors.forename: Christopher R
authors.initials: CR
authors.lastname: McCartney
mesh_terms: D050154:Adiposity; D000293:Adolescent; D000367:Age Factors; D001827:Body Height; D001835:Body Weight; D002648:Child; D005260:Female; D006801:Humans; D017588:Hyperandrogenism / Q000209:etiology / Q000503:physiopathology; D006946:Hyperinsulinism / Q000209:etiology / Q000503:physiopathology; D007333:Insulin Resistance; D008297:Male; D009765:Obesity / Q000150:complications* / Q000503:physiopathology; D011085:Polycystic Ovary Syndrome / Q000209:etiology / Q000503:physiopathology; D011627:Puberty; D011628:Puberty, Delayed / Q000209:etiology* / Q000503:physiopathology; D011629:Puberty, Precocious / Q000209:etiology* / Q000503:physiopathology; D013997:Time Factors
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