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Insulin-Like Growth Factor Binding Protein-I Levels Are Strongly Associated with Insulin Sensitivity and Obesity in Early Pubertal Children¹

Division of Endocrinology, Department of Pediatrics, The Children’s Hospital (S.H.T.), Division of Biostatistics (B.W.J.), and The Center for Human Nutrition and Division of Endocrinology, Metabolism and Diabetes, Department of Medicine (R.H.E.), University of Colorado Health Sciences Center, Denver, Colorado 80262; and Division of Endocrinology, Department of Pediatrics (J.I.L., S.E.G., R.G.R.), Oregon Health Sciences University, Portland, Oregon, 97201

Address all correspondence and requests for reprints to: Sharon H. Travers, Division of Endocrinology, B-265, The Children’s Hospital, 1056 E. 19th Avenue, Denver, Colorado 80218.

In conditions associated with insulin resistance, insulin-like growth factor binding protein-I (IGFBP-I) levels have been shown to correlate inversely with insulin levels. Puberty is associated with insulin resistance and thus provides a model for comparing the relationship of IGFBP-I to both insulin levels and measures of insulin sensitivity. Our study population consisted of 104 healthy pubertal children, age 9.8–14.6 yr. Each subject had his/her insulin sensitivity (Si) assessed by the modified minimal model of Bergman, which employs a frequently sampled iv glucose tolerance test. Results showed that IGFBP-I levels were significantly higher in boys than in pubertally matched girls (P < 0.01). There was a strong positive correlation between IGFBP-I levels and Si (r = 0.65, P < 0.0001) and a weaker negative correlation with fasting insulin levels (r = -0.38, P < 0.0001). An inverse relationship was also found between IGFBP-I levels and body mass index (r = -0.46, P < 0.0001) and with IGF-I levels (girls only, r = -0.41, P < 0.003). Consequently, insulin sensitivity, obesity, and IGF-I are important predictors of IGFBP-I levels in pubertal children. It is possible that insulin-mediated suppression of IGFBP-I in obese children may increase free IGF-I levels and thus contribute to somatic growth. The same mechanism may operate in pubertal children, where insulin resistance and growth acceleration occur simultaneously.

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