Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 832-836 |
| Number of pages | 5 |
| Journal | Journal of Clinical Endocrinology and Metabolism |
| Volume | 72 |
| Issue number | 4 |
| DOIs | |
| State | Published - Jan 1 1991 |
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ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Biochemistry
- Endocrinology
- Clinical Biochemistry
- Biochemistry, medical
Cite this
Insulin resistance : An early metabolic defect of turner’s syndrome. / Caprio, Sonia; Boulware, Susan; Diamond, Michael Peter; Sherwin, Robert S.; Carpenter, T. O.; Rubin, Karen; Amiel, Stephanie; Press, Martin; Tamborlane, William V.
In: Journal of Clinical Endocrinology and Metabolism, Vol. 72, No. 4, 01.01.1991, p. 832-836.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Insulin resistance
T2 - An early metabolic defect of turner’s syndrome
AU - Caprio, Sonia
AU - Boulware, Susan
AU - Diamond, Michael Peter
AU - Sherwin, Robert S.
AU - Carpenter, T. O.
AU - Rubin, Karen
AU - Amiel, Stephanie
AU - Press, Martin
AU - Tamborlane, William V.
PY - 1991/1/1
Y1 - 1991/1/1
N2 - 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.
AB - 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.
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U2 - 10.1210/jcem-72-4-832
DO - 10.1210/jcem-72-4-832
M3 - Article
VL - 72
SP - 832
EP - 836
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
SN - 0021-972X
IS - 4
ER -