title: Cortisol treatment affects glucocorticoid receptor and glucocorticoid-responsive genes in the liver of rainbow trout.
abstract: We investigated whether longer-term cortisol exposure modified hepatic glucocorticoid receptor (GR) status and tissue responsiveness to cortisol stimulation in rainbow trout. Fish were given intraperitoneal implants of cortisol (50mg/kg body mass) and this led to elevated plasma cortisol levels mimicking chronically stressed salmonids. There was significantly higher hepatic GR mRNA abundance, despite a drop in GR protein content in the liver of cortisol-treated fish. The tissue responsiveness to cortisol stimulation was apparent from the higher plasma glucose concentration and liver glycogen content. Also, the higher phosphoenolpyruvate carboxykinase (PEPCK) mRNA abundance, a key glucocorticoid-responsive gene, by cortisol suggests activation of the GR signalling pathway. There was no significant effect of cortisol treatment on liver PEPCK, alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase activities compared to the sham fish. The higher heat shock protein (hsp) 90 mRNA abundance and a corresponding elevation in this protein and constitutive hsp70 (hsc70) protein content in the cortisol-treated fish reflects a role for glucocorticoids in the hepatic stress response process. Taken together, the molecular and biochemical responses evident in the liver of trout imply changes favouring tissue responsiveness to glucocorticoids and may be a mechanism to offset GR protein downregulation evident with chronic cortisol stimulation in rainbow trout.
authors.affiliation: Department of Biology, University of Waterloo, Waterloo, Ont., Canada N2L 3G1.mvijayan@sciborg.uwaterloo.ca
authors.forename: Mathilakath M
authors.initials: MM
authors.lastname: Vijayan
authors.forename: Stavroula
authors.initials: S
authors.lastname: Raptis
authors.forename: Ramesh
authors.initials: R
authors.lastname: Sathiyaa
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001786:Blood Glucose / Q000378:metabolism; D015153:Blotting, Western; D017931:DNA Primers; D015870:Gene Expression / Q000187:drug effects*; D005938:Glucocorticoids / Q000494:pharmacology*; D050883:HSC70 Heat-Shock Proteins; D018840:HSP70 Heat-Shock Proteins / Q000096:biosynthesis / Q000235:genetics; D018841:HSP90 Heat-Shock Proteins / Q000096:biosynthesis / Q000235:genetics; D006854:Hydrocortisone / Q000494:pharmacology*; D008099:Liver / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism*; D008112:Liver Glycogen / Q000378:metabolism; D017686:Oncorhynchus mykiss / Q000235:genetics*; D019764:Phosphoenolpyruvate Carboxykinase (ATP) / Q000378:metabolism; D011506:Proteins / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis; D011965:Receptors, Glucocorticoid / Q000187:drug effects*; D012015:Reference Standards
chemical_list: D000893:Anti-Inflammatory Agents; D001786:Blood Glucose; D017931:DNA Primers; D005938:Glucocorticoids; D050883:HSC70 Heat-Shock Proteins; D018840:HSP70 Heat-Shock Proteins; D018841:HSP90 Heat-Shock Proteins; D008112:Liver Glycogen; D011506:Proteins; D012333:RNA, Messenger; D011965:Receptors, Glucocorticoid; D019764:Phosphoenolpyruvate Carboxykinase (ATP); D006854:Hydrocortisone