New evidence for a role of melatonin in glucose regulation

被引：103

作者：

Peschke, Elmar ^{[1
]}

Muehlbauer, Eckhard ^{[2
]}

机构：

[1] Univ Halle Wittenberg, Inst Anat & Cell Biol, D-06097 Halle, Germany

[2] Saxon Acad Sci Leipzig, D-04107 Leipzig, Germany

来源：

BEST PRACTICE & RESEARCH CLINICAL ENDOCRINOLOGY & METABOLISM | 2010年 / 24卷 / 05期

关键词：

Insulin; melatonin; melatonin receptors MT1 and MT2; cAMP; cGMP and IP3; type 1-and type 2-diabetes; PANCREATIC BETA-CELLS; PROTEIN-COUPLED-RECEPTORS; FASTING PLASMA-GLUCOSE; CGMP SIGNALING PATHWAY; MOUSE PARS TUBERALIS; INSULIN-SECRETION; CIRCADIAN RESPONSES; GENE-EXPRESSION; COMMON VARIANT; INCREASED RISK;

D O I：

10.1016/j.beem.2010.09.001

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Glucose triggers insulin secretion of the pancreatic beta-cells. The pineal hormone melatonin interferes in this process by inhibiting secretion and transmitting circadian timing information to the islets. Circadian insulin secretion is adapted to day/night changes through melatonin-dependent synchronization. In rats and mice, melatonin levels are high during the dark period, which is their active feeding period, while, in humans, melatonin levels are high during the overnight fasting and sleeping period. This implies a different read-out of melatonin signaling in day-active species, including man. Dysregulation of circadian secretion may be a key to the increase of type 2 diabetes (T2D). This review discusses the impact of melatonin on insulin secretion transmitted through both the pertussis-toxin-sensitive membrane receptors MT1 (MTNR1a) and MT2 (MTNR1b) and the second messengers cAMP, cGMP and IP3. This is an important topic since, in several genetic association studies, single nucleotide polymorphisms of the human MT2-receptor have been described as being causally linked with an elevated risk of developing T2D. This article summarizes interrelationships between melatonin and insulin in type 1 diabetic (T1D) and type 2 diabetic (T2D) rats and humans. (C) 2010 Elsevier Ltd. All rights reserved.

引用

页码：829 / 841

页数：13

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