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Assessment of Child Anthropometry in a Large Epidemiologic Study
Published on: February 2, 2017
Advanced bone age and hyperinsulinemia in overweight and obese children
Orit Pinhas-Hamiel1, Doreen Benary2, Kineret Mazor-Aronovich1
1Pediatric Endocrinology and Diabetes Unit, Edmond and Lily Safra Children's Hospital, Sheba Medical Center, Tel Hashomer, Israel Sackler School of Medicine, Tel-Aviv University, Israel.
Insights
Marked hyperinsulinemia is associated with advanced bone age (BA) in obese children. This suggests insulin may directly influence skeletal growth in humans, impacting bone maturation.
Area of Science:
- Pediatric Endocrinology
- Metabolic Syndrome Research
- Skeletal Development Studies
Background:
- Obese children often exhibit advanced bone age (BA) compared to chronological age (CA).
- In vitro studies suggest insulin may directly impact skeletal growth.
- The relationship between insulin levels and BA maturation in obese children requires investigation.
Purpose of the Study:
- To investigate the association between fasting insulin levels and bone age maturation in obese children.
- To determine if insulin modulates skeletal growth in this population.
Main Methods:
- A cohort of 74 overweight and obese children (ages 4-13) was studied.
- Bone age advancement was assessed using the BA divided by CA ratio (BA:CA).
- Metabolic syndrome components, including fasting insulin, were measured.
Main Results:
- Advanced BA maturation (BA:CA > 1.21) was linked to younger age, higher BMI-Z scores, and increased height.
- Females had a significantly higher risk of advanced BA compared to males.
- Hyperinsulinemia (fasting insulin > 30 μU/L) was independently associated with a 6.8-fold increased risk of advanced BA.
Conclusions:
- Significant hyperinsulinemia is associated with advanced bone age in obese children.
- These findings suggest insulin plays a role in modulating skeletal growth in humans.
Objective:
In obese children, bone age (BA) tends to significantly exceed chronological age (CA). In vitro studies in mice suggest that insulin may directly modulate skeletal growth. We investigated whether there is an association between fasting insulin and BA maturation in obese children.
Methods:
The study cohort comprised 74 overweight and obese children ages 4 to 13 years. BA divided by CA was used as an index for bone advancement. Participants were classified into tertiles based on their BA:CA ratio. Advanced BA maturation was defined as the third tertile, with BA:CA > 1.21. Components of the metabolic syndrome, including fasting insulin, fasting glucose, triglycerides, and high-density lipoprotein (HDL) levels, were measured.
Results:
Children with advanced BA were significantly younger, had a higher body mass index (BMI)-Z score (BMI-Z), and were taller than children with bone advancement in the lower tertiles. Females had a 4.7-fold increased risk for advanced BA compared with males (95% confidence interval [CI], 1.29-17.1; P = .02). Children with a BMI-Z ≥ 1.96 and fasting insulin ≤ 30 μU/L had a 3.6-fold increased risk of advanced BA (95% CI, 1.00-12.8; P = 0.05). Moreover, hyperinsulinemia (fasting insulin > 30 μU/L) was associated with a 6.8-fold increased risk for advanced BA, independent of the degree of obesity (95% CI, 1.45-32.1; P = .01).
Conclusion:
Marked hyperinsulinemia is associated with advanced BA in obese children. Insulin appears to modulate skeletal growth in humans.
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