Rat Model of Food-induced Non-obese-type 2 Diabetes Mellitus: Comparative Pathophysiology and Histopathology

Overview

Journal Int J Physiol Pathophysiol Pharmacol

Date 2012 Mar 31

PMID 22461957

Citations 11

Authors

Akindele O Adeyi

Babatunde A Idowu

Chiedu F Mafiana

Samuel A Oluwalana

Oluwasola L Ajayi

Oluseyi A Akinloye

Affiliations

Soon will be listed here.

Abstract

Based on the hypothesis that consistent hyperglycemia can result in insulin resistance, we explored the induction of non-insulin dependent diabetes mellitus (NIDDM) using diet of high glycemic/low fat index and compared the effects on the physiology and histology of the rats. The rats were divided into 3 groups. DM was induced in the first group by single intraperitoneal injection of 150mg/kg alloxan monohydrate and in the second group by feeding the rats with diet of high glycemic index/low fat for 8 weeks. The pathophysiology and histopathology of DM were studied. Hyperglycemia was recorded in the alloxan and food-induced groups respectively. Both groups were also positive for glycosuria, which confirmed the induction of DM. Concentrations of plasma potassium, calcium, protein and urea were higher (p<0.05) in the alloxan-induced than the food-induced diabetic rats, whereas food-induced rats recorded higher hematological indices than the alloxan-induced group. Coronary risk indices were higher in food-induced diabetic rats than the alloxan-induced, while activities of antioxidant enzymes were significantly higher (p<0.05) in alloxan-induced diabetic rats than the food-induced rats. Marked degenerations of the Islets of Langerhans was observed in pancreas of alloxan-induced diabetic rats, whereas, histological examination of the pancreas of food-induced and control rats revealed no visible lesion. Liver and kidney of all food and alloxan-induced diabetic rats showed marked degeneration of the hepatocytes and the glomeruli respectively. This study presents a rat model of type II diabetes mellitus using food of high glycemic/low fat index with its consequent ionoregulatory disruptions, acute anemia, hyperlipidemia, nephropathy and hepatopathy.

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