Characterisation of subjects with early abnormalities of glucose tolerance in the Stockholm Diabetes Prevention Programme:: the impact of sex and type 2 diabetes heredity

被引:69
作者
Kuhl, J [1 ]
Hilding, A
Östenson, CG
Grill, V
Efendic, S
Båvenholm, P
机构
[1] Karolinska Inst, Dept Mol Med, S-17176 Stockholm, Sweden
[2] Karolinska Hosp, Dept Med, S-10401 Stockholm, Sweden
关键词
glucose intolerance; insulin secretion; insulin sensitivity; type 2 diabetes heredity;
D O I
10.1007/s00125-004-1614-1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Aims/hypothesis: We evaluated the impact of sex and type 2 diabetes heredity on the prevalence and pathogenesis of early abnormalities of glucose homeostasis in subjects participating in the Stockholm Diabetes Prevention Programme. Methods: A sample of 3,128 men and 4,821 women, of whom approximately half had a family history of type 2 diabetes (FHD) was categorised according to an OGTT: NGT, IFG, IGT, combined glucose intolerance and type 2 diabetes. The homeostasis model assessment was used to determine insulin sensitivity and beta cell function. Results: Prevalence of early abnormalities of glucose metabolism was two to three times higher in subjects with FHD and two to three times higher in men compared to women. Both maternal and paternal heredity of type 2 diabetes were associated with an increased risk of having early abnormalities of glucose metabolism. However, in women with type 2 diabetes heredity on the fathers side seems to have less impact on an increased risk of having type 2 diabetes. Both waist circumference and systolic blood pressure were increased in subjects with abnormalities of glucose homeostasis, whereas insulin sensitivity and beta cell function were decreased. Subjects with IFG had more pronounced impairment of beta cell function and insulin sensitivity than subjects with IGT. Conclusion/interpretation: An FHD and male sex increased the prevalence of abnormalities of glucose homeostasis. Subjects with IFG had more pronounced defects of insulin secretion and action than subjects with IGT.
引用
收藏
页码:35 / 40
页数:6
相关论文
共 29 条
[1]   Work stress and low sense of coherence is associated with type 2 diabetes in middle-aged Swedish women [J].
Agardh, EE ;
Ahlbom, A ;
Andersson, T ;
Efendic, S ;
Grill, V ;
Hallqvist, J ;
Norman, A ;
Östenson, CG .
DIABETES CARE, 2003, 26 (03) :719-724
[2]  
[Anonymous], 1985, World Health Organ Tech Rep Ser, V727, P1
[3]   ASSOCIATION OF INSULIN AND INSULIN PROPEPTIDES WITH AN ATHEROGENIC LIPOPROTEIN PHENOTYPE [J].
BAVENHOLM, P ;
KARPE, F ;
PROUDLER, A ;
TORNVALL, P ;
CROOK, D ;
HAMSTEN, A .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1995, 44 (11) :1481-1488
[4]   Insulin sensitivity of suppression of endogenous glucose production is the single most important determinant of glucose tolerance [J].
Båvenholm, PN ;
Pigon, J ;
Östenson, CG ;
Efendic, S .
DIABETES, 2001, 50 (06) :1449-1454
[5]  
Borch-Johnsen K, 1999, LANCET, V354, P617
[6]   Low birth weight, family history of diabetes, and glucose intolerance in Swedish middle-aged men [J].
Carlsson, S ;
Persson, PG ;
Alvarsson, M ;
Efendic, S ;
Norman, A ;
Svanström, L ;
Östenson, CG ;
Grill, V .
DIABETES CARE, 1999, 22 (07) :1043-1047
[7]  
Carlsson S, 1998, AM J EPIDEMIOL, V148, P539, DOI 10.1093/oxfordjournals.aje.a009679
[8]   The 1997 American Diabetes Association criteria versus the 1985 World Health Organization criteria for the diagnosis of abnormal glucose tolerance - Poor agreement in the Hoorn study [J].
De Vegt, F ;
Dekker, JM ;
Stehouwer, CDA ;
Nijpels, G ;
Bouter, LM ;
Heine, R .
DIABETES CARE, 1998, 21 (10) :1686-1690
[9]   FASTING HYPERGLYCEMIA IN NON-INSULIN-DEPENDENT DIABETES-MELLITUS - CONTRIBUTIONS OF EXCESSIVE HEPATIC GLUCOSE-PRODUCTION AND IMPAIRED TISSUE GLUCOSE-UPTAKE [J].
DEFRONZO, RA ;
FERRANNINI, E ;
SIMONSON, DC .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1989, 38 (04) :387-395
[10]   THE DISPOSAL OF AN ORAL GLUCOSE-LOAD IN HEALTHY-SUBJECTS - A QUANTITATIVE STUDY [J].
FERRANNINI, E ;
BJORKMAN, O ;
REICHARD, GA ;
PILO, A ;
OLSSON, M ;
WAHREN, J ;
DEFRONZO, RA .
DIABETES, 1985, 34 (06) :580-588