Abstract

Objective To investigate the effects of acyl and deacyl ghrelin on the expressions of PI3Kp85α,Akt/PKB and GLUT4,the key factors in insulin receptor signaling pathway of insulin resistance in skeletal muscle cells.Methods Insulin resistance models were made by palmitic acid induced rat L6 myoblasts.Successful models were divided into acyl ghrelin group,deacyl ghrelin group,PI3K inhibitor(LY) + acyl ghrelin group,LY + deacyl ghrelin group and control group with corresponding interventions for 24h.The glucose uptake of all group was measured through laser confocal microscopy and flow cytometry.Expressions of phosphorated/total PI3Kp85α,phosphorated/total Akt and cell membrane/total GLUT4 of skeletal muscle cells were measured by Western blot,and PI3Kp85α,Akt,GLUT4 mRNA expression were detected by real-time PCR.Results Induced L6 myoblasts differentiation and insulin resistance model were successfully established.Acyl and deacyl ghrelin could increase glucose uptake for 1.25 and 1.28 folds compared to control group,and the phosphorated and total PI3Kp85α expressions were 1.78 and 1.89 folds to control group,and phosphorylated/total Akt and cell membrane/total GLUT4 were 1.84 and 1.80 folds to control group.The PI3Kp85α,Akt/PKB and GLUT4 mRNA expression were also upregulated compared to control group.The above indexes of LY + acyl or deacyl ghrelin group decreased significantly compared to acyl and deacyl ghrelin group without LY.Conclusions Acyl and deacyl ghrelin can both improve insulin resistance in skeletal muscle cells,increasing the glucose uptake under insulin-stimulation,and up-regulated the phosphorated PI3Kp85α,phosphorated Akt/PKB,and cell membrane GLUT4 relative protein expressions and mRNA expressions.PI3K inhibitor,LY294002,can inhibit the above improvement effect of acyl and decyl ghrelin. Key words: Insulin resistance of skeletal muscles; Ghrelin; PI3K-Akt/PKB pathway

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.