title: Elevated brain glucose and glycogen concentrations in an animal model of depression.
abstract: BACKGROUND
  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.
  
  
  CONCLUSIONS
  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. © 2014 S. Karger AG, Basel.
authors.affiliation: Department of Experimental Neuroendocrinology, Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland.
authors.forename: Jan
authors.initials: J
authors.lastname: Detka
authors.forename: Anna
authors.initials: A
authors.lastname: Kurek
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Basta-Kaim
authors.forename: Marta
authors.initials: M
authors.lastname: Kubera
authors.forename: Władysław
authors.initials: W
authors.lastname: Lasoń
authors.forename: Bogusława
authors.initials: B
authors.lastname: Budziszewska
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism*; D003345:Corticosterone / Q000378:metabolism; D003866:Depressive Disorder / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D005947:Glucose / Q000008:administration & dosage / Q000378:metabolism*; D051272:Glucose Transporter Type 1 / Q000378:metabolism; D051274:Glucose Transporter Type 3 / Q000378:metabolism; D051275:Glucose Transporter Type 4 / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism; D008297:Male; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011897:Random Allocation; D017207:Rats, Sprague-Dawley; D011972:Receptor, Insulin / Q000378:metabolism; D013315:Stress, Psychological / Q000378:metabolism*
chemical_list: D051272:Glucose Transporter Type 1; D051274:Glucose Transporter Type 3; D051275:Glucose Transporter Type 4; D007328:Insulin; C495679:Slc2a1 protein, rat; C495690:Slc2a3 protein, rat; C495694:Slc2a4 protein, rat; D006003:Glycogen; D011972:Receptor, Insulin; D005947:Glucose; D003345:Corticosterone