Blood sugar dysregulation damages learning and memory

More evidence for the deleterious effects on the brain of hyperglycemia and hypoglycemia is presented in a study just published in the journal Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. The authors' research was designed to...

"...evaluate the effects of streptozotocin (STZ)-induced hyperglycemia and insulin-induced hypoglycemia in cortical and hippocampal mitochondria bioenergetics and oxidative status."

The hippocampus is the seat of short-term memory and a regulatory center for adrenal function. STZ-induced hyperglycemia and insulin-induced hypoglycemia are standard methods employed to examine the physiological repercussions of high and low blood sugar respectively. They analyzed the respiratory chain and phosphorylation system for the capacity to produce energy in the mitochondria (cellular energy 'factories'), thiobarbituric acid reactive substances (TBARS) levels and the hydrogen peroxide (H2O2) production rate for oxidative stress, and non-enzymatic and enzymatic antioxidant defenses. What did their data show?

"Cortical mitochondria from insulin-induced hypoglycemic rats present a significant decrease in the ADP/O index, a significant increase in the repolarization lag phase and a decrease in GSH/GSSG ratio when compared with STZ and control mitochondria. Both STZ-induced diabetes and insulin-induced hypoglycemia promote a significant increase in TBARS levels and a decrease in glutathione disulfide reductase activity. Diabetic cortical mitochondria present a significant decrease in glutathione peroxidase (GPx) activity compared to control mitochondria. In turn, insulin-induced hypoglycemia induced a significant increase in GPx and manganese superoxide dismutase (MnSOD) activities. In hippocampal mitochondria, insulin-induced hypoglycemia increases the respiratory control ratio whereas both situations, hyper- and hypoglycemia, potentiate H2O2 production and decrease the activity of MnSOD."

In other words, both hyper- and hypoglycemia impair cortical and hippocampal function deranging energy production, increasing damage due to oxidative stress. In reference to type 1 diabetes, the authors state in conclusion:

"These results suggest that the poor glycemic control that occurs in type 1 diabetic patients undergoing insulin therapy may have detrimental effects in brain areas involved in learning and memory."