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Pediatric Endocrinology |
Department of Pediatrics (P.L.H., W.S.C., P.D.G.) and the Health Research Council Biostatistics Unit, Department of Community Health (E.M.R.), University of Auckland, Auckland, New Zealand; the Department of Physiology and Biophysics, University of Southern California (R.N.B.), Los Angeles, California 90089; and the Department of Endocrinology, Childrens Hospital of Pittsburgh (R.K.M., M.A.S.), Pittsburgh, Pennsylvania 15260
Address all correspondence and requests for reprints to: Dr. Wayne Cutfield, Department of Pediatrics, University of Auckland, Private Bag 92019, Auckland, New Zealand.
Epidemiological studies have demonstrated an association between intrauterine growth retardation and an increased risk of adult diseases that include essential hypertension, noninsulin-dependent diabetes mellitus, and ischemic heart disease. A common feature of these diseases is insulin resistance.
To investigate whether abnormal insulin sensitivity was a characteristic of subjects with intrauterine growth retardation (IUGR), we compared two groups of short prepubertal children: a group with IUGR (birth weight less than the tenth percentile; n = 15) and a normal birth weight group (n = 12). Subjects underwent a modified frequently sampled iv glucose tolerance test that permitted calculation of the acute insulin response, insulin sensitivity index, and glucose effectiveness.
A marked difference in the insulin sensitivity index was noted between groups, with the IUGR group being less insulin sensitive [6.9 vs. 16.9 10-4 min-1·(µU/mL); P = 0.0048]. The acute insulin response was also significantly different between groups, with IUGR subjects having higher insulin levels (445 vs. 174 µU/mL; P = 0.005). There was no difference in glucose effectiveness between groups.
Short prepubertal IUGR children have a specific impairment in insulin sensitivity compared to their normal birth weight peers. In short IUGR children, impaired insulin sensitivity is a potential marker for the early identification and intervention in the development of late adult-onset noninsulin-dependent diabetes mellitus.
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