Objective: Stress has been linked to several diseases. In the course of stress; blood sugar. cortisol and catecholamine levels increase. Visceral hypersensitivity will increase due to catecholaminergic discharges leading to an over-induction of the intrapancreatic secretion. A chronically stress has a role in the induction of insulin resistance in different tissues and pancreas begins to release excessive insulin causing burned out pancreas. For this reason, it becomes insulin insufficiency, elevated blood sugar and risk of type 2 diabetes.
Aim: In this study, our aim was to investigate the histopathologic influence of stress on the pancreas at light microscopic level on the rat model.
Methods: Animals were divided into two groups, stressed and control (n=4/group). Rats of the stressed group were exposed to Chronic mild stress (CMS) model of depression for 2 weeks. During the experiment, rats were given food and tap water ad libitum. At the end of the test, rats were slept with ketamin HCI and sacrificed. The pancreas was totally removed with opening the abdomens and fixed with 10% formaldehyde for histopathological evaluation. Tissue samples were blocked in paraffin blocks. The prepared 5-μ thickness sections were stained with haematoxylineosin and examined by light microscopy.
Results: Our histological observations have showed disruption of normal configuration of serous acini in pancreatic tissue sections of the stress-exposed animals in comparation with the control group. The borders of the acini were broken down and there were cytoplasmic vacuolations in aciner cells. Additionally, shrunken, apoptotic and necrotic acini were seen together. In stressed animals, sinusoidal dilatation and cellular degeneration were observed in the islets of Langerhans. Mononuclear cell infiltrations in the perivascular areas and vacuolations in the vascular wall were determined in the interlobular connective tissue of the pancreas.
Conclusions: According to our data, CMS can lead to evident damage in the microscopic structure of pancreas. At the same time, this case may effect negatively pancreas physiology and cause to the onset diabetes.
Acknowledgement: This study was supported by the 2008/20-numbered Scientific Research Fund of our University.
25 - 29 Apr 2009
European Society of Endocrinology