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Neu-p11 Improve Insulin Sensitivity In Insulin Resistant 3t3-l1 Adipocytes

Posted on:2011-08-01Degree:MasterType:Thesis
Country:ChinaCandidate:X X WangFull Text:PDF
GTID:2154360308977492Subject:Biochemistry and Molecular Biology
Abstract/Summary:PDF Full Text Request
Objective: To investigate the effect of Neu-P11 on improving insulin sensitivity in insulin resistant 3T3-L1 adipocyte, and to study the mechanism of Neu-P11 and Mel improving insulin sensitivity in insulin resistant 3T3-L1 adipocytes.Methods: 1. 3T3-L1 pre-adipocytes were differentiated into adipocytes by IBMX, DEX and insulin and determined by oil red O staining. 2. Insulin resistant 3T3-L1 adipocytes were induced in DMEM with high glucose / high insulin for 24 hours, TG concentration and glucose consumption was detected by enzymatic method to evaluate the model. 3. Effect of Mel and Neu-P11 on glucose consumption, insulin sensitivity and TG concentration were studied and related proteins were detected by western-blot.Results: 1. 3T3-L1 pre-adipocytes were differentiated into adipocytes after 10-12 days, and the cells changed from fusiform to round. 2. After adipocytes were induced in DMEM with high glucose / high insulin for 24h, the glucose consumption decreased significantly and the TG concentration increased significantly compared with normal adipocytes. 3. After insulin resistant adipocytes treated with Mel and Neu-P11, the glucose consumption, insulin sensitivity and the expression of APN increased significantly, the TG content decreased significantly, but the expression of Leptin and AdipoR1 had no significant change, neither did the phosphorylation of AMPK and ACC.Conclusions: 1.High glucose / high insulin can induce adipocytes developing into insulin resistant adipocytes. 2. Neu-P11 can significantly increase glucose consumption, insulin sensitivity and expression of APN and decrease TG content. 3. Mel and Neu-P11 had no significant effects on expression of Leptin / AdipoR1 and the phosphorylation of AMPK / ACC. So we infer that they improve the glucose and lipid metabolism disorder via other signal pathway.
Keywords/Search Tags:Neu-P11, high glucose/high insulin, 3T3-L1 cells, insulin resistance, AMPK
PDF Full Text Request
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