Hypercortisolemia In the streptozotocin-diabetic Gerbils (Gerbillus Gerbillus)

Abstract

One of the recognized issues in diabetes mellitus research is the lack of animal models allowing the research of pathological, biochemical and genetic factors in immuno-competent animals. Our research group has successfully employed the gerbil in several studies of experimental diabetes and hypercaloric diet. In the present work, we investigate the effect of an acute and chronic pharmacologic stress, the streptozotocin (STZ) induced diabetes type I, in the gerbillus gerbillus. In this purpose, we aimed to study the morphology of the gerbil's adrenal gland with assessment of cortisol level at two and 30 days of diabetes. Adult gerbils weighing 25–28 g (n = 11), were divided into the following groups: non-diabetic (control), 2 days of diabetes (acute) and 30 days of diabetes (chronic). The experimental groups received an intra-peritoneal injection of a single dose of 150 mg/kg STZ. At two and 30 days of diabetes the animals underwent a retro-orbital puncture, for assessment of hormonal parameters (Cortisol and insulin) and subsequently decapitated, the adrenal glands were removed, weighed and processed for light microscopy and stereology. Non-diabetic control gerbils with citrate buffer were also examined for comparison. At two days of diabetes, STZ gerbils – adrenal gland showed a significant increase in weight, accompanied by a larger cortex layer, hypertrophy of the fasciculate cells and a significant decrease in the nucleocytoplasmic index, these changes were associated with higher plasma cortisol level, compared to non-diabetic controls. At 30 days post-diabetes, cortisol level remained elevated compared to control; whereas it decreased significantly compared to the early stage of diabetes. These data indicate that, the administration of STZ involve in the small gerbil, an endocrine and metabolic dysfunction as well as structural disorders of the adrenal cortex that could be a sign of hyperactivity at the early stage of the disease and suggest a possible reduction in adrenocortical sensitivity over time.