Neu-p11 reduces clock/apelin expression in insulin-resistant mouse adipocyte model

• 来源期刊: 生物化学与生物物理学报（英文版）
• 年，卷（期）: 2013,（9）
• 页码范围: 798-800
• 页数: 3页
• 语种: 英文
• DOI: 10.1093/abbs/gmt077

摘要

It is generally accepted that a major risk factor of type 2 diabetes mellitus (T2DM) is insulin resistance and is often associated with obesity [1].Apelin (expressed in adipose tissue) appears as a beneficial adipokine with anti-diabetic and antiobesity properties [2].Clock is a large and complex gene encoding a novcl mcmber of the basic helix-loop-helix/ Per-ARNT-Sim protein family of transcription factors.Circadian clocks can regulate metabolic homeostasis and clock disruption leads to obesity and the metabolic syndrome [3].Melatonin (Mel) is an integral part of the homeostatic mechanism in the body.It is best known as a regulator of seasonal and circadian rhythms,with high expression level during the night and low level during the day.Interestingly,insulin levels are also adapted to day/night changes through Mel-dependent synchronization.Mel may influence diabetes and be associated with metabolic disturbances by regulating insulin secretion [4].Luzindole is the non-specific Mel receptor antagonist that can block some functions of Mel [5].Although Mel has a wide range of biological effects,studies have found that once it gets into human body,its metabolism can be very fast,with a half-life of 20-30min.Therefore,apparent effects cannot be achieved from direct administration of this medicine.