Pancreatic beta-cell function and insulin sensitivity in Japanese subjects with impaired glucose tolerance and newly diagnosed type 2 diabetes mellitus

被引:31
|
作者
Kanauchi, M
Nakajima, M
Saito, Y
Kanauchi, K
机构
[1] Nara Med Univ, Dept Internal Med 1, Kashihara, Nara 6340813, Japan
[2] Sharp Co Ltd, Med Ctr Employees Hlth, Shimjo, Japan
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 2003年 / 52卷 / 04期
关键词
D O I
10.1053/meta.2003.50078
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
To clarify whether pancreatic beta-cell function and/or insulin resistance contributes to development of glucose intolerance in Japanese subjects, we investigated 551 subjects who underwent a 75-g oral glucose tolerance test (OGTT). Subjects were divided into 3 groups: normal glucose tolerance (NGT, n = 238), impaired glucose tolerance (IGT, n = 211), and newly diagnosed type 2 diabetes mellitus (n = 102). The diabetics were subdivided into 3 subgroups as follows: diabetes with normal fasting glucose (fasting plasma glucose [FPG] < 110 mg/dL), diabetes with impaired fasting glucose (FPG < 110 to 125 mg/dL), and diabetes with diabetic fasting glucose (FPG greater than or equal to 126 mg/dL). Insulinogenic index as early-phase insulin secretion, homeostasis model assessment (HOMA-beta and HOMA-resistance), and 4 different formulas of insulin sensitivity index were assessed by plasma glucose and insulin concentrations obtained at fasting or during a 75-g OGTT. Both early-phase insulin secretion and insulin sensitivity were low even in the IGT stage compared with NGT. The transition from IGT to diabetes was accompanied by a progressive deterioration of insulin reserve as well as insulin resistance. During the further progression in diabetes, insulinogenic index decreased additionally, whereas declines in insulin sensitivity were relatively small. In conclusion, both impaired insulin secretion and insulin resistance may contribute to the underlying mechanisms of glucose intolerance in Japanese subjects. Copyright 2003 Elsevier, Inc. All rights reserved.
引用
收藏
页码:476 / 481
页数:6
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