Aggravated dyslipidemia in diabetic albino rats after subchronic oral aluminium chloride exposure

Background. Diabetes mellitus causes fasting hyperglycemia and dyslipidemia, and exposure of diabetics to aluminium can aggravate these effects, since aluminium exposure also causes prediabetic hyperglycemia and dyslipidemia. The effect has not been previously demonstrated in an animal model. Aim. Objective of the study was to determine the extent of aggravation of dyslipidemia after subchronic oral exposure of diabetics (type 1 model in rat) to aluminium chloride.Method. Forty adult male rats (weighing 189–285 g) were divided into four groups of ten rats each: Control group (CG); Aluminium chloride (Al) treated group (AG); Diabetic group (DG); Al-treated-diabetic group (ADG). Diabetes was induced by single intramuscular injection of aqueous alloxan monohydrate (100 mg/ml) at 120 mg/kg in DG and ADG. Each rat in the Al-treated groups (AG and ADG) was orally administered with aqueous aluminium chloride (100 g/L) daily (50 mg/kg; 12.5% of LD₅₀) by gavage for 28 days. Fasting blood glucose (FBG) and serum total cholesterol (TC), triglyceride (TG) and high density lipoprotein cholesterol (HDLc) concentrations were determined. Low density lipoprotein cholesterol (LDLc) and atherogenic index of plasma (AIP) were calculated with formulae. Results. Diabetic hyperglycemia was maintained in DG and did not differ from ADG on day 7–21, but was higher (p < 0.05) on day 28 in association with aggravated dyslipidemia characterized by increases in TG, TC, LDLc, AIP and decrease in HDLc. Conclusion. Subchronic aluminium exposure in diabetics aggravated hyperglycemia and dyslipidemia with AIP elevation by 34%, suggesting an exaggeration of risk of atherogenesis, atherosclerosis and cardiovascular disease.