Background and Aim: Diabetes Mellitus is a prevalent metabolic disease, which is caused by deficiency in insulin secretion or malfunction of a series of agents affecting its function. Diabetic hyperglycemia and hyperlipidemia can induce many structural and functional disturbances in all body systems. The aim of the present study was to identify histochemical liver tissue changes in diabetes mellitus in Rats as an experimental model.
Materials and Methods: A total number of 60 male Sprague Dawley Rats with the average weight of 250±20 gr were chosen and divided into two experimental (45) and control (15) groups. Each of these groups was then divided into three subgroups of 2, 8, and 16-weeks. All the rats were put in a standard condition with respect to temperature, humidity, darkness and lighting periods availability of water and food stuff. The experimental group developed diabetes through receiving I.P. injection of 60mg/kg of streptozotocin. Rats in the control group received the same amount of normal saline. In due course, liver specimens were taken from both groups. Tissue specimens were processed routinely and paraffin blocks prepared then, the dissected tissues were stained by Hematoxylin Eosin, PAS, PNA/Alcian blue pH=2.5. Lectin (10 microgram/mL) was diluted with Buffer phosphate (pH=6.6).
Results: The study showed very little presence of disaccharide galactose/ install galactosamine in bile subendothelial ducts and in the center of lobule venule in the diabetic group. PAS staining showed an increase in the quantity of glycogen particles in peripherally located hepatocytes of liver cell lobule especially in the 16 week subgroup. Besides, liver congestion was observed in the diabetic groups.
Conclusion: It seems that liver tissue changes in diabetic groups is time dependent and could be seen in blood vessels, bile duct epithelium and hepatocytes. Further studies will probably show the role of these changes in pathogenesis of diabetes mellitus.
Type of Study:
Original Article |
Subject:
Histology Received: 2006/09/6 | Accepted: 2016/03/10 | ePublished: 2016/03/10