No abstract

Introduction: Recent data indicate that there is a link between depression and diabetes and that excess glucocorticoids may play an underlying role in the pathogenesis of both of these diseases. The aim of the present study was to determine whether there are any alterations in glucose, glycogen, glucose transporters, insulin, insulin receptors or corticosterone concentrations in the hippocampus and frontal cortex in a prenatal stress rat model of depression. Methods: Male rats whose mothers had been subjected to stress and control animals were subjected to the Porsolt test to verify the experimental model. Next, some of the rats were subjected to acute stress and/or were administered glucose. Glucose, glycogen, corticosterone, insulin, insulin receptor, phospho-insulin receptor and glucose transporter (GLUT1, GLUT3 and GLUT4) concentrations were assayed. Results: Prenatally stressed rats exhibited glucose and glycogen concentrations in both investigated brain structures that exceeded those of the control animals. Prenatal stress also increased the levels of glucose transporters - GLUT1 in both tissues and GLUT4 in the frontal cortex. The changes in the prenatally stressed rats were more prominent in the animals that were subjected to stress or glucose loading in adulthood. Conclusion: The increase in carbohydrate brain concentrations evoked by prenatal stress may result from changes in the amounts of glucose transporters, especially GLUT1. Moreover, the obtained results support the hypothesis that stress during the perinatal period permanently increases the sensitivity of brain tissue to factors that act in adulthood.

Clinical studies have indicated a frequent coexistence of depression and diabetes. Both of these diseases are associated with similar changes in the structure and function of the central nervous system cells and with similar disturbances of cognitive processes. Some morphological and functional changes occurring in these diseases seem to result from exaggerated glucocorticoid, proinflammatory cytokine or glutamate action. Glucocorticoids induced by stress are known not only to affect synaptic plasticity but also to disturb brain glucose metabolism and decrease insulin sensitivity. Functional neuroimaging studies demonstrated altered glucose metabolism in the brains of depressed patients. Changes in the amount or activity of key metabolic enzymes and a lower sensitivity of insulin receptors have been detected in the brains of animal models of both of these diseases. Hence, excess glucocorticoids can lead to impaired insulin action and glucose metabolism, to limited energy supply for proper neuronal function and, consequently, to disturbed synaptic plasticity.