Impact of metabolic abnormalities for beta cell function: Clinical significance and underlying mechanisms

被引：12

作者：

Grill, V. ^{[1
]}

Bjorklund, A. ^{[2
]}

机构：

[1] Univ Trondheim Hosp, Dept Internal Med, N-7006 Trondheim, Norway

[2] Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden

来源：

MOLECULAR AND CELLULAR ENDOCRINOLOGY | 2009年 / 297卷 / 1-2期

关键词：

Insulin secretion; Islets of Langerhans; Diabetes; Diazoxide; Beta cell; Fatty acids; Transplantation; INDUCED INSULIN-SECRETION; LOW-DENSITY-LIPOPROTEIN; FREE FATTY-ACIDS; HUMAN PANCREATIC-ISLETS; LONG-TERM EXPOSURE; CHRONIC HYPERGLYCEMIA; UNCOUPLING PROTEIN-2; DIAZOXIDE TREATMENT; IN-VITRO; GLUCOSE;

D O I：

10.1016/j.mce.2008.06.009

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

It is firmly established that poor metabolic control in diabetes inhibits beta cell function. Chronic hyperglycaemia is probably the most important factor, exerting both primary negative effects (by glucose per se and/or metabolites) and secondary ones (by beta cell exhaustion). Dyslipidemia in diabetes aggravates the glucose effects both by inducing insulin resistance and by direct effects on beta cells. Much experimental and some clinical evidence indicates that therapies that promote "beta cell rest" such as early and intensive insulin treatment and K-ATP channel blockers can be beneficial. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

引用

页码：86 / 92

页数：7

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