The beta cell lesion in type 2 diabetes: there has to be a primary functional abnormality

被引：219

作者：

Kahn, S. E. ^{[1
]}

Zraika, S. ^{[1
]}

Utzschneider, K. M. ^{[1
]}

Hull, R. L. ^{[1
]}

机构：

[1] VA Puget Sound Hlth Care Syst 151, Dept Med, Div Metab Endocrinol & Nutr, Seattle, WA 98108 USA

来源：

DIABETOLOGIA | 2009年 / 52卷 / 06期

关键词：

Amyloid; Animal models; Beta cell function; Beta cell mass; Beta cell volume; Genes; Glucagon; Insulin secretion; Islets; Pancreatectomy; IMPAIRED GLUCOSE-TOLERANCE; GLUCAGON-LIKE PEPTIDE-1; INSULIN-SECRETION; PARTIAL PANCREATECTOMY; ENDOCRINE PANCREAS; B-CELLS; A-CELLS; ISLET; PROINSULIN; MELLITUS;

D O I：

10.1007/s00125-009-1321-z

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The critical role of the beta cell in the pathogenesis of type 2 diabetes is now well established. When examined in patients with type 2 diabetes and individuals at increased risk, reductions in beta cell mass and abnormalities of beta cell function can both be demonstrated. The question of whether one alone is sufficient or both are necessary for the development of hyperglycaemia has been debated. Based on human and animal studies, it appears that neither alone is sufficient. Rather, for glucose to rise to the level at which diabetes would be diagnosed, defects in beta cell mass and in beta cell function are required.

引用

页码：1003 / 1012

页数：10

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