
Vol. 65, No. 2, 2006
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Winner of the ESPE-Hormone Research Prize Free access
Original Paper
Insulin Resistance Is an Intrinsic Defect Independent of Fat Mass in Women with Turner's Syndrome
Burak Salgina, Rakesh Amina, Kevin Yuena, Rachel M. Williamsa, Peter Murgatroydb, David B. Dungera
aUniversity Department of Paediatrics, and bWellcome Trust Clinical Research Facility, University of Cambridge, Cambridge, UK
Address of Corresponding Author
Horm Res 2006;65:69-75 (DOI: 10.1159/000090907)
Key Words
- Turner's syndrome
- Insulin resistance
- Body composition
Abstract
Background/Aims: Turner's syndrome (TS) is associated with increased insulin resistance and adiposity, which might be associated with type 2 diabetes in later life. We aimed to determine whether the defect in insulin sensitivity is a primary intrinsic defect in TS or dependent on variation in body composition. Methods: Sixteen women with TS not on growth hormone replacement but receiving oestrogen replacement therapy [age (mean ± SD): 30.2 ± 8.5 years; height-corrected fat-free mass: 26.1 ± 3.1 kg/height] and a control group of 16 normal healthy women (age: 30.1 ± 8.2 years; height-corrected fat-free mass: 25.9 ± 2.4 kg/height) were studied. Fasting blood samples were obtained for measurement of glucose, insulin, IGF-I, IGFBP-1, IGFBP-3 and lipid levels. The hyperinsulinaemic euglycaemic clamp was performed to assess peripheral insulin sensitivity (M value), and the Homeostasis Model Assessment (HOMA-S) was used to estimate fasting insulin sensitivity. Body composition was assessed using a dual-energy X-ray absorptiometry scan. Results: Fasting insulin sensitivity (HOMA-S 103.2 ± 78.6 vs. 193.9 ± 93.5, p = 0.006) was lower in TS subjects compared to controls as was whole-body insulin sensitivity (M value 2.9 ± 1.9 vs. 5.5 ± 2.6 mg/kg/min, p = 0.003). In a multiple regression analysis the Turner karyotype was significantly related to insulin sensitivity (p = 0.008) independent of any differences in fat-free mass and percent whole-body fat mass. Conclusion: The increased insulin resistance in women with TS is independent of measures of body composition and may represent an intrinsic defect related to their chromosomal abnormality. Copyright © 2006 S. Karger AG, Basel
Author Contacts
Prof. David B. Dunger University Department of Paediatrics, University of Cambridge Addenbrooke's Hospital, Level 8, Box 116 Cambridge CB2 2QQ (UK) Tel. +44 1223 336 886, Fax +44 1223 336 996, E-Mail dbd25@cam.ac.uk
Article Information
Received: August 3, 2005
Accepted: November 7, 2005
Published online: January 10, 2006
Number of Print Pages : 7
Number of Figures : 1, Number of Tables : 4, Number of References : 45 |
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