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Subject Area

Physiology

Article Type

Original Study

Abstract

Objective: To investigate the impact of type 2 diabetes milletus on glycemic state, cognitive brain function, and hippocampus DNA in adult male rats as well as potential underlying mechanisms.

Background: It has been predicted that the number of diabetics will more than likely double by the year 2030 as a result of urbanization, obesity, and ageing. Diabetes mellitus is linked to the onset of dementia and Alzheimer's disease.

Methods: Thirty-six male albino rats of local strain, at 6 weeks of age weighing 150 - 200 gm each, were divided into 2 equal groups: non-Diabetic and Diabetic non-treated groups. After 4 weeks (the experimental period), rats were tested for non-spatial and spatial memory and learning. Glycemic state, lipid profile, Malondialdehyde, total antioxidant capacity and Interleukin-6 were measured in serum. The tissue of right hippocampus was assessed for degeneration by histopathological examination with measurement of the intensity of expression of phosphorylated tau by immunohistochemistry. RNA, intact DNA and DNA fragmentation were assessed in tissue of the left hippocampus.

Results: Induction of type 2 diabetes in rats resulted in significant hyperglycemia, dyslipidemia, oxidative stress, significant decline in cognitive brain functions (non-spatial and spatial memory and learning) with hyperphosphorylation of tau and DNA fragmentation when compared to non-diabetic group.

Conclusion: Type 2 Diabetes Milletus resulted in impairment of cognitive brain function as it caused nucleic acid damage and hyperphosphorylation of tau; a marker for brain neurodegeneration. This can be explained by hyperglycaemia, dyslipidaemia, oxidative stress and the enhanced inflammatory state.

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