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The N -acetylaspartate network begins in neurons with N -acetylaspartate production catalyzed by aspartate N -acetyltransferase from acetyl-CoA and aspartate. Clinical studies reported a significant depletion in N -acetylaspartate brain level in type 1 diabetic patients. The main goal of this study was to establish the impact of either hyperglycemia or oxidative stress on the N -acetylaspartate network. For the in vitro part of the study, embryonic rat primary neurons were treated by using a nitric oxide generator for 24 h followed by 6 days of post-treatment culture, while the neural stem cells were cultured in media with 25-75 mM glucose. For the in vivo part, male adult Wistar rats were injected with streptozotocin (65 mg/kg body weight, ip) to induce hyperglycemia (diabetes model) and euthanized 2 or 8 weeks later. Finally, the biochemical profile, NAT8L protein/ Nat8l mRNA levels and enzymatic activity were analyzed. Ongoing oxidative stress processes significantly affected energy metabolism and cholinergic neurotransmission. However, the applied factors did not affect the N -acetylaspartate network. This study shows that reduced N -acetylaspartate level in type 1 diabetes is not related to oxidative stress and that does not trigger N -acetylaspartate network fragility. To reveal why N -acetylaspartate is reduced in this pathology, other processes should be considered.

Neither Excessive Nitric Oxide Accumulation nor Acute Hyperglycemia Affects the N-Acetylaspartate Network in Wistar Rat Brain Cells