Endocrine Abstracts

Background: Diabetes Mellitus (DM) is an endocrine disorder resulting in hyperglycaemia that affects many vital organs of the body like the brain. The molecular mechanisms underlying dementia, memory loss and cognition dysfunction caused by DM are still not very clear. CD47 is a cell surface protein working in the homeostasis of the immune system. The causal relationship of CD47 has been shown in neurodegenerative diseases. CD47 also has a role in pancreatic islet cells and their maintenance in T1DM models.

Aim: Tha aims of the study are to determine cognitive funcitons in healthy and diabetic mice, to examine CD47 expression in brain tissue of healthy and diabetic mice and to determine its relationship with cognitive functions in T1DM and T2DM mice models.

Methods: This study was done using 39 CD1 male mice which were grouped as control (n=12), T1DM (n=11) and T2DM (n=16). T1DM and T2DM were induced by streptozocin and high-fat diet, respectively. Glucose levels of 200mg/dl or higher at the 2nd hour of oral glucose tolerance test established the diagnosis of DM in the T2DM group. Blood glucose of the mice was measured from the tail tip blood every week in all groups. Cognition tests {Control Open Field (COF) test, Y-Maze test, Novel Object Recognition (NOF) tests] were conducted to evaluate the animals’ (control and type 1 DM group) cognitive functions. After sacrification, immunofluorescent staining and imaging were done to investigate the expression of CD47 in hippocampus region of brain tissue (in all 3 groups).

Results: The cognitive scores in the 2 out of 3 tests (COF, P=0.03; NOR, P=0.01,; Y-Maze, P=NS) in the T1DM group were significantly lower compared to the controls. CD47 expression was increased in both the T1DM and T2DM mice compared to controls (P=0.014). No correlation was observed between CD47 expression and cognitive functions in the T1DM mice.

Conclusion: Cognitive scores are decreased in T1DM mice compared to controls. CD47 expression is increased in the brains of diabetic mice compared to controls. There does not seem to be any correlation of CD47 expression and cognitive functions in diabetic mice. The explanation may be that CD47 levels in the brain may be elevated as a way of cells to protect themselves from excess blood glucose independent of cognitive functions.