Comparative Effects of Experimental Diabetes Mellitus and Glucocorticoid-Induced Hypercortisolemia on Pancreatic and Adrenal Endocrine Architecture: A Pathological Study in Rats

Abstract

Diabetes mellitus (DM) and hypercortisolemia are closely associated endocrine disorders that significantly affect glucose metabolism; however, their direct organ-specific interactions remain incompletely understood. This study aimed to comparatively evaluate the effects of experimental DM on the adrenal gland and glucocorticoid-induced hypercortisolemia on the pancreas. Thirty male Wistar albino rats were allocated into three groups: control, DM (streptozotocin, 20 mg/kg), and hypercortisolemia (prednisolone, 10 mg/kg/day) for 30 days. Postprandial glucose levels were measured. Pancreatic and adrenal tissues were examined using histopathological and immunohistochemical methods to assess insulin, glucagon, and insulin receptor expression. Both experimental conditions were associated with histopathological alterations in endocrine tissues. The DM group exhibited degenerative changes in pancreatic islets, while the hypercortisolemia group showed structural alterations in both pancreatic islets and adrenal cortex. Immunohistochemical analysis revealed reduced insulin and insulin receptor expression in both groups. Postprandial glucose levels were significantly elevated (p<0.001), including in the hypercortisolemia group, supporting the hyperglycemic effect of glucocorticoid exposure. These findings suggest that both DM and glucocorticoid excess are associated with structural and functional alterations in endocrine tissues. These findings suggest that both DM and glucocorticoid excess are associated with parallel structural and functional alterations in endocrine tissues, rather than indicating a direct bidirectional interaction. Further molecular studies are required to clarify the underlying mechanisms and causal relationships. These findings highlight that each condition induces structural alterations in the reciprocal endocrine organ, suggesting cross-organ vulnerability under metabolic stress.