Insulin facilitates glucose transporter 4 gene expression in canine heart in vivo / 免疫学杂志

Objective　To investigate the mechanism for that insulin facilitates increase of glucose uptake. Methods　The expression of myocardial GLUT4 polypeptide was determined by semiquantitative immunoblotting. The expression of GLUT4 mRNA was determined by semiquantitative Northern blotting. Results　After infusing insulin for 8　hours，the　expression　of　GLUT4 mRNA and GLUT4 polypeptide was significantly higher in canine myocardium than in　those　found normal ones. The glucose uptake was upregulated at　the　same　time．Conclusions　Our findings suggest that insulin facilitates the expression of GLUT4 mRNA and GLUT4 polypeptide in canine hearts. Enhanced GLUT4 expression is one of the important molecular mechanism by which myocardial cells enhance glucose uptake by insulin stimulation.

Additive e ffects of hyperinsulinemia and ischemia on canine myocardial GLUT4 gene expression in vivo / 第二军医大学学报

Objective: To investigate whether there is additi ve effects of hyperinsulinemia and ischemia on expression of canine myocardial G LUT4 gene in vivo. Methods: The expression of myocardial GLU T4 was determined by semiquantitative immunoblotting.The expression of GLUT4 mRN A was determined by semiquantitative Northern blotting. Results: Dramatic changes were seen in GLUT4 mRNA and GLUT4 expression in the ischemic hearts.After infusing insulin for 8 h,regional GLUT4 mRNA and GLUT4 levels in is chemic hearts were 2.5, 2.3-fold that of expression in normal hearts(P<0.01 ). Myocardial glucose uptake in ischemic hearts was increased by 4-fold when co mpared with normal hearts(P<0.01). Conclusion: There are not only additive effects of hyperinsulinemia and low-flow ischemia on canine myoc ardial GLUT4 mRNA and GLUT4 expression in vivo, but also increase of myocar dial glucose uptake. Enhanced GLUT4 expression may be an important protective m echanism by which myocardial cells enhance glucose uptake and metabolism during low-flow ischemia.

Insulin enhances glucose transporter 1 gene expression of low-flow ischemic myocardium / 中国病理生理杂志

AIM: To investigate the mechanism underlying insulin-stimulated increase in glucose uptake during low-flow myocardial ischemia. METHODS: The expression of myocardial GLUT1 polypeptide was determined by semiquantitative immunoblotting. The expression of GLUT1 mRNA was determined by semiquantitative Northern blotting. RESULTS: After infusing insulin during low- flow myocardial ischemia for 8 h，the expression of both GLUT1 mRNA and GLUT1 polypeptide was significantly higher in experimental myocardium than that in normal myocardium. The glucose uptake was upregulated at the same time in the exprimental myocardium. CONCLUSION: Insulin enhances the expression of GLUT1 mRNA and GLUT1 polypeptide in ischemic myocardial regions. GLUT1 expression may be an important mechanism by which myocardial cells enhance glucose uptake and metabolism during low-flow myocardial ischemia.

Insulin enhances glucose transporter 1 gene expression of low-flow ischemic myocardium / 中国病理生理杂志

AIM: To investigate the mechanism underlying insulin-stimulated increase in glucose uptake during low-flow myocardial ischemia. METHODS: The expression of myocardial GLUT1 polypeptide was determined by semiquantitative immunoblotting. The expression of GLUT1 mRNA was determined by semiquantitative Northern blotting. RESULTS: After infusing insulin during low- flow myocardial ischemia for 8 h,the expression of both GLUT1 mRNA and GLUT1 polypeptide was significantly higher in experimental myocardium than that in normal myocardium. The glucose uptake was upregulated at the same time in the exprimental myocardium. CONCLUSION: Insulin enhances the expression of GLUT1 mRNA and GLUT1 polypeptide in ischemic myocardial regions. GLUT1 expression may be an important mechanism by which myocardial cells enhance glucose uptake and metabolism during low-flow myocardial ischemia. [