Effects of Type 1 and Type 2 Diabetes on Micro-Anatomical Changes of Adrenal Gland in Male Wistar Rats

Background & Aims: Changing the hormonal output of endocrine glands, diabetes leads to the occurrence of secondary metabolic disorders. Neuropathy, on the other hand, is the most common neurological complication of diabetes which affects the neuroendocrine system, in addition to peripheral and autonomic nervous system, contributing to exacerbation of disease severity. In this line, the present study was conducted to comparatively evaluate the effects of hyperglycemia, induced by experimental type 1 and type 2 diabetes, on micro-anatomical changes of adrenal gland in male Wistar rats. Methods: Eighteen male Wistar rats were allocated into three groups including control (healthy), experimental type 1 diabetes (subcutaneous injection of 135mg/kg alloxan), and experimental type 2 diabetes (treated with drinking water containing 10% fructose for 8 weeks). Two months after the induction of both types of diabetes, levels of blood biochemical factors such as glucose, insulin, cortisol, triglycerides, cholesterol, LDL and HDL were measured. One of the adrenal glands was randomly removed from each rat and, following tissue preparation and staining, was evaluated in terms of structural changes of the adrenal cortex and medulla using stereological techniques. Results: Serum biochemical and hormonal analysis indicated a significant difference in levels of glucose, triglycerides, insulin and cortisol between control and experimental groups. The results achieved by the evaluation of adrenal volume showed increased volume of adrenal cortex in type 1 and type 2 diabetes and also reduced volume and neuronal density of adrenal medulla in type 1 diabetes compared with control. Conclusion: Due to increased activity of hypothalamic-pituitary-adrenal axis, enhanced ACTH secretion in diabetes-induced hyperglycemia leads to increased growth of adrenal cortex and secretion of adrenal hormones. Reduced volume and neuronal density of adrenal medulla in diabetic condition may be resulted from the development of abnormal metabolic pathways such as those in hyperglycemia-derived oxidative stress. Late incidence of structural and functional impairments in type 2 diabetes can be ascribed to occurrence rate of hyperglycemia and insulin resistance, and, thus, the disease complications largely depend on the disease duration.