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Insulin Resistance: An Early Metabolic Defect of Turner's Syndrome^*

SONIA CAPRIO, SUSAN BOULWARE, MICHAEL DIAMOND, ROBERT S. SHERWIN, T. O. CARPENTER, KAREN RUBIN, STEPHANIE AMIEL, MARTIN PRESS and WILLIAM V. TAMBORLANE

Departments of Pediatrics, Internal Medicine, and Obstetrics and Gynecology, and the Clinical Research Center, Yale University School of Medicine New Haven, Connecticutt 06510

Address requests for reprints to: Dr. Sonia Caprio, Section of Pediatric Endocrinology, Department of Medicine, Yale University School of Medicine, P.O. Box 3333, New Haven, Connecticutt 06510–8064.

Recipient of a Career Development Award from the Juvenile Diabetes Foundation International.

To evaluate whether insulin resistance contributes to the increased risk of diabetes in patients with Turner's syndrome, we measured insulin sensitivity (using the euglycemic insulin clamp technique, 40 mU/m² · min) and whole body glucose and lipid oxidation (assessed by indirect calorimetry) in two groups of nondiabetic patients with Turner's syndrome and age-matched normal controls. Group 1 consisted of eight young patients (mean age, 10 ± 0.8 yr) who had never received hormone therapy, and group 2 consisted of five patients (mean age, 17.6 ± 1.4 yr) who had been or were on estrogen therapy. In group 2, [3-³H]glucose was also infused during the euglycemic clamp to assess hepatic sensitivity to insulin. During the euglycemic clamp, insulin-stimulated glucose metabolism was decreased in both groups of patients [group 1, 8.4 ± 1.0 vs. 14.7 ± 2 mM/m² · min in controls (P < 0.05); group 2, 9 ± 0.7 vs. 11.7 ± 0.9 mM/m²·min in controls (P < 0.05)]. The impairment of insulin-stimulated glucose metabolism in patients with Turner's syndrome was accounted for by reduced nonoxidative glucose disposal; glucose oxidation rose to a similar extent in Turner patients and normal controls. Insulin-induced suppression of hepatic glucose production (group 2) and plasma FFA and branched chain amino acid levels in Turner patients was also indistinguishable from that in normal controls. Our data suggest that in patients with Turner's syndrome, insulin resistance is a very early metabolic defect that may be restricted to nonoxidative pathways of intracellular glucose metabolism. (J Clin Endocrinol Metab 72: 832–836, 1991)

^* This work was supported by grants from the NIH (RR-00125 and DK-20495).

Received May 11, 1990.

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