Early Pubertal Development and Insulin Sensitivity among School-Aged Girls: Mediation Via Adiposity
Cincinnati Children's Hospital Medical Center, Division of Adolescent Medicine and University of Cincinnati College of Medicine, Cincinnati, OH. Electronic address: .Journal of pediatric and adolescent gynecology (Impact Factor: 1.68). 11/2012; 26(1). DOI: 10.1016/j.jpag.2012.09.007
STUDY OBJECTIVE: To examine whether the known association between early pubertal breast maturation and insulin sensitivity (SI) is mediated by adiposity. DESIGN: Cross-sectional analyses. SETTING: Observational study examining the roles of environment, diet, and obesity on puberty. PARTICIPANTS: 379 girls with a mean age, 7.03 years; 62% were white and 29% black. MAIN OUTCOME MEASURES: Pubertal development was assessed via physical examination and adiposity by body mass index Z score (BMI Z) and waist-to-height ratio. Fasting blood samples were obtained for insulin and glucose concentrations. SI was calculated with the quantitative insulin sensitivity check index (QUICKI). Analysis of variance and Sobel's test was used to assess mediation. RESULTS: Fifty-five girls were pubertal (Tanner 2 breast). Breast maturation was inversely associated with SI (P = .005) and positively associated with BMI Z (P < .001) and waist-to-height ratio (P < .001). The effect of breast maturation on SI was no longer significant (P = .41) after adjusting for the effect of BMI Z, which remained significant (P < .001). Similar results were obtained when waist-to-height ratio replaced BMI Z in the models. Mediation analyses demonstrated that 75% of the association between breast maturation and SI is mediated by adiposity. CONCLUSIONS: In girls, decreased SI during early puberty is largely mediated by total and visceral adiposity.
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ABSTRACT: Leptin is a permissive factor for the onset of puberty. However, changes in adiposity frequently influence leptin sensitivity. Thus, the objective of the present study was to investigate how changes in body weight, fatness, leptin levels and leptin sensitivity interact to control the timing of puberty in female mice. Pre-pubertal obesity, induced by raising C57BL/6 mice in small litters, led to an early puberty onset. Inactivation of Socs3 gene in the brain or exclusively in leptin receptor-expressing cells reduced the body weight and leptin levels at pubertal onset, and increased leptin sensitivity. Notably, these female mice exhibited significant delays in vaginal opening, first estrus and onset of estrus cyclicity. In conclusion, our findings suggest that increased leptin sensitivity did not play an important role in favoring pubertal onset in female mice. Rather, changes in pubertal body weight, fatness and/or leptin levels were more important in influencing the timing of puberty.
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