Wen-Tung Wang1, Phil Lee1,2,
Irina V Smirnova3, In-Young Choi1,4
1Hoglund Brain Imaging
Center, University of Kansas Medical Center, Kansas City, KS, United States; 2Molecular
& Integrative Physiology, University of Kansas Medical Center, Kansas
City, KS, United States; 3Physical Therapy & Rehabilitation
Sciences, University of Kansas Medical Center, Kansas City, KS, United
States; 4Neurology, University of Kansas Medical Center, Kansas
City, KS, United States
Acute uncontrolled hyperglycemia results in significant increases in osmolytes. In chronic stage, osmolarity dysregulation indicated by plateau levels of osmolytes leads to significant reduction of Ala, Asp, GSH, and NAA. This study explores effects of chronic hyperglycemia on neurochemical profile and glucose transport. The results show that acute glycemic normalization restores alterations in all metabolites except Ala, Ins, and NAA. The remained reduction in NAA level indicates that neuronal damage caused by hyperglycemia can not be reversed. The relationsip between plasma and brain glucose concentration of STZ-induced diabetic rats indicates an un-altered glucose transport.
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