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日本糖耐量受损和新诊断2型糖尿病患者的胰岛β细胞功能及胰岛素敏感性

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

作者信息

Kanauchi Masao, Nakajima Mikane, Saito Yoshihiko, Kanauchi Kimiko

机构信息

First Department of Internal Medicine, Nara Medical University, Kashihara, Japan.

出版信息

Metabolism. 2003 Apr;52(4):476-81. doi: 10.1053/meta.2003.50078.

DOI:10.1053/meta.2003.50078
PMID:12701062
Abstract

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 >or= 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.

摘要

为了阐明胰岛β细胞功能和/或胰岛素抵抗是否与日本人群糖耐量异常的发生有关,我们对551名接受75克口服葡萄糖耐量试验(OGTT)的受试者进行了研究。受试者被分为3组:糖耐量正常(NGT,n = 238)、糖耐量受损(IGT,n = 211)和新诊断的2型糖尿病(n = 102)。糖尿病患者又被细分为3个亚组:空腹血糖正常的糖尿病患者(空腹血糖[FPG]<110mg/dL)、空腹血糖受损的糖尿病患者(FPG为110至125mg/dL)以及糖尿病空腹血糖的糖尿病患者(FPG≥126mg/dL)。通过空腹或75克OGTT期间测得的血糖和胰岛素浓度,评估作为早期胰岛素分泌的胰岛素生成指数、稳态模型评估(HOMA-β和HOMA-抵抗)以及4种不同公式的胰岛素敏感性指数。与NGT相比,即使在IGT阶段,早期胰岛素分泌和胰岛素敏感性也较低。从IGT到糖尿病的转变伴随着胰岛素储备以及胰岛素抵抗的逐渐恶化。在糖尿病的进一步发展过程中,胰岛素生成指数进一步下降,而胰岛素敏感性的下降相对较小。总之,胰岛素分泌受损和胰岛素抵抗可能都与日本人群糖耐量异常的潜在机制有关。

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