Fasting hyperglycaemia, glucose intolerance and pancreatic islet necrosis in albino rats associated with subchronic oral aluminium chloride exposure

Exposure to aluminium is associated with altered glycaemia, but this effect in relation to glucose tolerance and pancreatic islet pathology requires validation. The study was aimed at assessing the glycaemic changes, glucose tolerance and islet morphology of albino rats during oral aluminium chloride exposure. Twenty male albino rats weighing 189–270 g were randomly divided into two equal groups. The control group was sham-treated with normal saline and the treated group was administered aluminium chloride solution (100 g/L) by gavage at 12.5% of LD50 (50 mg/kg) daily for 28 days. Fasting blood glucose (FBG) and postprandial blood glucose (PBG) concentrations after glucose gavage at 1 g/kg were estimated and the pancreatic islet tissues were examined for histopathological changes. The treatment caused significant (p < 0.05) time-dependent (r = 0.97) increases in FBG. Hyperglycaemic effect was estimated to be 28-day glycaemic increase of 61% and aggregate glycaemic increases of 44% and 53% between and within groups, respectively. Oral glucose tolerance was impaired judging by changes in PBG which indicated reduction of both intestinal absorption and clearance of blood glucose in treated group by 37% and 17%, respectively. Coagulative necrosis and 31% reduction (p < 0.05) in cell count of the pancreatic islet tissue were associated with the deranged circulatory glucose homeostasis in the treated group. In conclusion, aluminium loading seems to affect insulin production and action and may have a contributory role in diabetogenesis.