Caffeine-induced Expression Of GLUT4 Relationship Between STZ Diabetic Rat Skeletal Muscle Cells And Caused Protein CaMKII And HDAC5

Objective：In normal rats and diabetic rats caused by STZ stimulus given motionsimulation signal-caffeine, detection of the phosphorylation levels of CaMK ⅡandHDAC5phosphorylation levels and GLUT4protein expression levels in skeletal musclecell, so as to study CaMK Ⅱ and HDAC5protein change and the relationship betweenGLUT4expression, especially in the diabetic condition under the influence.Methods: Adult male wistar rats48, were randomly divided into normal group (n=24) and the result of STZ diabetic model group (n=24). Normal group subdivided intocaffeine injections based experimental group (MC), without caffeine injections of2minutes from the control group (M), caffeine injections based group (HC), withoutcaffeine injection based on control group24hours (H); Caused by STZ diabetic modelgroup as above: the caffeine injections based experimental group2minutes (DMC),with no caffeine injection2minutes from the control group (DM) and caffeineinjections (DHC) based group,24hours without caffeine injections (DH) based controlgroup24hours a day.2minutes from animal samples using western blot method todetect proteins of skeletal muscle cells CaMK Ⅱ (Thr286) phosphorylation level andHDAC5(Ser259) phosphorylation and (Ser498) phosphorylation levels,24hours basedanimal samples using western blot method to determine the amount of skeletal musclecell protein GLUT4protein expression level.Results: Normal and diabetic rats were respectively the same trend: after injection ofcaffeine, the phosphorylation levels of the proteins CaMK Ⅱ (Thr286)、HDAC5(Ser498) andHDAC5(Ser259) in skeletal muscle cell of normal and diabetic ratsand GLUT4protein expression levels were significantly higher than their respectivecontrol, and have significant difference.Among them, the CaMK Ⅱ (Thr286)phosphorylation level of normal animal experimental group is3.92times that of thecontrol group (P <0.05); Experimental HDAC5(Ser498) phosphorylation level4.2times higher than the control group (P <0.01, highly significant difference);Experimental group HDAC5(Ser259) phosphorylation level is1.29times (the controlgroup (P <0.05); Experimental group of GLUT4protein level was1.91times in thecontrol group (P <0.01, highly significant difference). In diabetes animal model, theinjection of Caffeine experimental CaMK Ⅱ (Thr286) level of phosphorylation is noCaffeine is1.92times that of the control group (P <0.05); Experimental group ofGLUT4protein level was1.52times in the control group (P <0.05), and diabetic ratscompared with normal animals without diabetes, Caffeine can lead to diabetic ratsgroup CaMK Ⅱ (Thr286), HDAC5(Ser498) and (Ser259) phosphorylation and GLUT4protein expression levels and normal animals almost all of these values, therewas no significant difference.Conclusions:(1) Both in normal animal and diabetes animal model in Caffeinecauses the experimental group significantly GLUT4protein expression in the process ofskeletal muscle cells caused by Caffeine CaMK Ⅱ (Thr286) phosphorylation level andHDAC5(Ser498) and HDAC5(Ser259) phosphorylation level is completely intopositive correlation, which corresponds to a positive correlation relation betweenincrease skeletal muscle cells the expression of GLUT4protein, from the two kinds ofmodel animal confirmed that Caffeine motion simulation signal, namely the Ca2+signal so cause GLUT4expression of skeletal muscle cells by Caffeine-Ca2+-CaMKⅡ-HDAC5access mechanism.(2) caused by Caffeine on diabetes animal model ofskeletal muscle cells of GLUT4expression effect and the effect of normal animal, therewas no significant difference showed that diabetes animal model on the regulation ofgene and protein expression of GLUT4movement signal path is normal, impairedinsulin and insulin receptor-PI3K signaling pathway is not influence caused by motionsimulation signal Caffeine so the expression of GLUT4protein, it is proved fromanother Angle CaMK Ⅱ to regulate the expression of GLUT4skeletal muscle cells byHDAC5only with the motor that caused by signaling pathways related to musclecontraction.