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胰岛素抵抗是特纳综合征女性中一种独立于脂肪量的内在缺陷。

Insulin resistance is an intrinsic defect independent of fat mass in women with Turner's syndrome.

作者信息

Salgin Burak, Amin Rakesh, Yuen Kevin, Williams Rachel M, Murgatroyd Peter, Dunger David B

机构信息

University Department of Paediatrics, University of Cambridge, Cambridge, UK.

出版信息

Horm Res. 2006;65(2):69-75. doi: 10.1159/000090907. Epub 2006 Jan 10.

DOI:10.1159/000090907
PMID:16407654
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.

摘要

背景/目的:特纳综合征(TS)与胰岛素抵抗增加和肥胖有关,这可能与晚年的2型糖尿病有关。我们旨在确定胰岛素敏感性缺陷是TS的原发性内在缺陷还是取决于身体成分的变化。

方法

研究了16名未接受生长激素替代但接受雌激素替代疗法的TS女性[年龄(平均±标准差):30.2±8.5岁;身高校正后的去脂体重:26.1±3.1kg/身高]和16名正常健康女性对照组(年龄:30.1±8.2岁;身高校正后的去脂体重:25.9±2.4kg/身高)。采集空腹血样以测量血糖、胰岛素、IGF-I、IGFBP-1、IGFBP-3和血脂水平。进行高胰岛素正常血糖钳夹试验以评估外周胰岛素敏感性(M值),并使用稳态模型评估(HOMA-S)来估计空腹胰岛素敏感性。使用双能X线吸收法扫描评估身体成分。

结果

与对照组相比,TS受试者的空腹胰岛素敏感性(HOMA-S 103.2±78.6对193.9±93.5,p = 0.006)较低,全身胰岛素敏感性(M值2.9±1.9对5.5±2.6mg/kg/min,p = 0.003)也较低。在多元回归分析中,特纳核型与胰岛素敏感性显著相关(p = 0.008),与去脂体重和全身脂肪百分比的任何差异无关。

结论

TS女性胰岛素抵抗增加与身体成分测量无关,可能代表与其染色体异常相关的内在缺陷。

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