A novel hippocampus metabolite signature in diabetes mellitus rat model of diabetic encephalopathy.

Diabetic encephalopathy (DE) is one of the chronic complications of diabetes. Even then, the molecular mechanism underlying DE remains unexplored. In this study, we have made an attempt to investigate the metabolic changes associated with the streptozocin (STZ)-induced cognitive dysfunction in the hippocampus of the rat model, a classical rodent model for DE, with the help of Gas Chromatography-Mass Spectrometry-based method. The STZ injections led to the rise of mean blood glucose levels in the diabetes mellitus (DM) group of rats as compared to the control (CON) group of rats throughout the experiment. However, we did not find any significant difference between the blood glucose levels of the DM & the CON groups of rats before the STZ injection. The results indicated a behavioral and morphological cognitive dysfunction in the DM groups of rats. The metabolomic investigation of these DE rats demonstrated a lower level of N-acetylaspartate and dihydroxyacetone phosphate accompanied by a higher level of homocysteine and glutamate as against the CON group of rats. The outcome of this study may unravel the underlying pathophysiological mechanism of DE. Also, the metabolomic data from this study may provide a platform for the development of DE biomarkers.