Bonnefond Amélie, Froguel Philippe
European Genomic Institute for Diabetes (EGID), Institut Pasteur de Lille, Centre national de la recherche scientifique (CNRS), Unité mixte de recherche (UMR) 8199, University of Lille, 1 Rue du Professeur Calmette, B.P. 245, F-59019, Lille Cedex, France.
Department of Genomics of Common Disease, School of Public Health, Hammersmith Hospital, Imperial College London, Du Cane Road, London, W12 0NN, UK.
Diabetologia. 2017 May;60(5):823-825. doi: 10.1007/s00125-017-4255-x. Epub 2017 Mar 17.
Genome-wide association studies have detected an association between type 2 diabetes risk and a non-coding SNP located in MTNR1B, the gene encoding melatonin receptor 2 (MT2). Melatonin regulates circadian rhythms and sleep and associates with metabolic disorders. However, the mechanisms underlying these actions are still unclear. Functional genomic, animal and clinical studies have not reached the same conclusions: while some studies have reported that decreased melatonin signalling increases type 2 diabetes risk, others have found the opposite. In this commentary, we have tried to provide an explanation for these contradictions and we suggest how the community may progress to reach a unified picture of the effect of melatonin and its signalling on type 2 diabetes.
全基因组关联研究已经检测到2型糖尿病风险与位于MTNR1B（编码褪黑素受体2，即MT2的基因）中的一个非编码单核苷酸多态性之间存在关联。褪黑素调节昼夜节律和睡眠，并与代谢紊乱相关。然而，这些作用背后的机制仍不清楚。功能基因组学、动物和临床研究尚未得出相同的结论：虽然一些研究报告称褪黑素信号减弱会增加2型糖尿病风险，但其他研究却得出了相反的结果。在这篇评论中，我们试图为这些矛盾提供一种解释，并提出该领域如何取得进展，以形成关于褪黑素及其信号对2型糖尿病影响的统一认识。
