| Objective:The objective of present study was to examine the influence of melatonin receptor agonist Neu-P11on improving insulin sensitivity in insulin resistance3T3-L1adipocyte, and to research the mechanism of the melatonin and its receptor agonist Neu-P11and the change of IRS-1, GLUT-4, APN, and to investigate the effect of melatonin receptor antagonist luzindole and melatonin, Neu-P11joint action in insulin resistance3T3-L1adipocytes.Methods:1.3T3-L1pre-adipocytes were differentiated in adipogenic cocktail by IBMX, DEX and insulin and identified by oil red O staining.2. Insulin resistance3T3-L1adipocytes were induced in DMEM with high glucose/high insulin for24hours, and glucose consumption was detected by enzymatic method to evaluate the model.3. Influence of melatonin and Neu-P11on glucose consumption, insulin sensitivity and IRS-1, GLUT-4, APN of associated proteins were detected by western-blot.Results:1.3T3-L1pre-adipocytes were differentiated into adipocytes after10-12days, and the cells changed from fusiform to round.2. After adipocytes were induced in DMEM with high glucose/high insulin for24h, the glucose consumption reduced obviously and insulin sensitivity also decreased compared with normal adipocytes.3. After insulin resistance adipocytes treated with melatonin and Neu-P11, the glucose consumption and the expression of IRS-1, GLUT-4, APN raised significantly, the insulin sensitivity was improved, but above-mentioned proteins had no marked change by comparison with IR after melatonin receptor antagonist luzindole and Neu-P11, melatonin joint action. Conclusions:1. Melatonin and its receptor agonist Neu-P11can raise glucose consumption, insulin sensitivity and expression of IRS-1, GLUT-4, APN.2. Melatonin receptor antagonist luzindole may block some actions in insulin resistance3T3-L1adipocyte of melatonin and Neu-P11such as improving the glucose consumption, the insulin sensitivity and the expression of IRS-1, GLUT-4, APN. Postgraduate:Xiu-ping Li (Biochemistry and Molecular Biology) Directed by Professor:Wei-dong Yin... |