Abstract
Previous studies have shown that the principal glucose transporter isoform within the blood-brain barrier (BBB) is GLUT1, and that GLUT1 mRNA is upregulated and immunoreactive GLUT1 protein is downregulated in rats with streptozocin (STZ)-induced experimental diabetes. The present studies investigate effects of insulin therapy on both GLUT1 mRNA and immunoreactive GLUT1 protein in brain capillaries isolated from control (CO), diabetic (DM), and insulin-treated diabetic (IR x) rats. The following variables were measured: serum glucose levels, rat brain capillary immunoreactive GLUT1 level by quantitative Western blotting, and rat brain capillary GLUT1 and actin mRNA levels by quantitative Northern blotting. Serum glucose levels were 6.4 ± 1.2, 30.3 ± 3.2, and 3.7 ± 1.7 mmol/L in CO, DM, and IR x rats, respectively. Brain capillary immunoreactive GLUT1 transporter protein level was 53% ± 13% of CO values in DM rats, and this value was unchanged with insulin treatment. GLUT1 mRNA level in rat brain was increased to 131% ± 8% of CO values in DM rats and was 80% ± 5% of CO values in IR x rats. In conclusion, short-term insulin therapy in rats with STZ-induced diabetes normalizes BBB GLUT1 mRNA level, but does not normalize depressed immunoreactive GLUT1 protein level.
Sign-in/Register to access full text options 
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 callDisclaimer: 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.
