Cerebral metabolism in streptozotocin-diabetic rats: an in vivo magnetic resonance spectroscopy study

Aims/hypothesis. It is increasingly evident that the brain is another site of diabetic end-organ damage. The pathogenesis has not been fully explained , but seems to involve an interplay between aberrant glucose metabolism and vascular changes. Vascular changes, such as deficits in cerebral, blood fl ow, could compromise cerebral energy metabolism. We therefore examined cere bral metabolism in streptozotocin-diabetic rats in vivo by means of localis ed P-31 and H-1 magnetic resonance spectroscopy. Methods. Rats were examined 2 weeks and 4 and 8 months after diabetes induc tion. A non-diabetic group was examined at baseline and after 8 months. Results. In P-31 spectra the phosphocreatine:ATP, phosphocreatine:inorganic phosphate and ATP:inorganic phosphate ratios and intracellular pH in diabe tic rats were similar to controls at all time points. In H-1 spectra a lact ate resonance was detected as frequently in controls as in diabetic rats. C ompared with baseline and 8-month controls 1H spectra did, however, show a statistically significant decrease in N-acetylaspartate:total creatine (-14 % and -23 %) and N-acetylaspartate:choline (-21 % and -17 %) ratios after 2 weeks and 8 months of diabetes, respectively. Conclusion/interpretation. No statistically significant alterations in cere bral energy metabolism were observed after up to 8 months of streptozotocin - diabetes. These findings indicate that cerebral blood flow disturbances i n diabetic rats do not compromise the energy status of the brain to a level detectable by magnetic resonance spectroscopy. Reductions in N-acetylaspar tate levels in the brain of STZ-diabetic rats were shown by H-1 spectroscop y, which could present a marker for early metabolic or functional abnormali ties in cerebral neurones in diabetes.