title: Diminished glucocorticoid tonus in obese strain (OS) chickens with spontaneous autoimmune thyroiditis: increased plasma levels of a physicochemically unaltered corticosteroid-binding globulin but normal total corticosterone plasma concentration and normal glucocorticoid receptor contents in lymphoid tissues.
abstract: Obese strain (OS) chickens afflicted with spontaneous autoimmune thyroiditis (SAT) display several signs of a general immune dysbalance, some of which may be related to altered endocrine mechanisms such as the glucocorticoid tonus. The latter is the combined result of corticosterone (CN) production, metabolism as well as excretion, and the binding of CN to corticosteroid binding globulin (CBG) and glucocorticoid receptors (GR). The present study deals with the comparative investigation of these parameters in OS and normal White Leghorn (NWL) chickens. The results obtained with radioimmunoassay for CN and radioligand saturation assays for plasma CBG as well as GR in the thymus were as follows: (1) both OS and NWL have equal total CN levels; (2) however, OS chickens exhibit elevated CBG levels, whereas the physicochemical parameters (equilibrium affinity, specificity spectrum) of CBG were equal in OS and NWL; (3) the GR capacities and affinities were equal in both OS and NWL throughout development until thymic involution. Similarly, the specificity, affinity, and sedimentation behaviour were equal in OS and NWL. (4) Furthermore, no differences were found in the response of OS and NWL splenocytes to the suppressive effect of glucocorticoids in vitro, also excluding postreceptor alterations at the cellular level in the OS. From these findings we conclude that the increased CBG levels, which are not compensated for by either increased CN plasma levels or by increased receptor capacities or affinities in lymphatic organs, represent a diminished glucocorticoid tonus in OS chickens. This may have immunoregulatory consequences which, in turn, may contribute to the development of SAT.
authors.affiliation: Institute for General and Experimental Pathology, University of Innsbruck, School of Medicine, Austria.
authors.forename: R
authors.initials: R
authors.lastname: Fässler
authors.forename: H
authors.initials: H
authors.lastname: Dietrich
authors.forename: G
authors.initials: G
authors.lastname: Krömer
authors.forename: S
authors.initials: S
authors.lastname: Schwarz
authors.forename: H P
authors.initials: HP
authors.lastname: Brezinschek
authors.forename: G
authors.initials: G
authors.lastname: Wick
mesh_terms: D000818:Animals; D002645:Chickens; D003345:Corticosterone / Q000097:blood*; D005938:Glucocorticoids / Q000502:physiology*; D009765:Obesity / Q000276:immunology / Q000503:physiopathology*; D011965:Receptors, Glucocorticoid / Q000378:metabolism*; D013045:Species Specificity; D013601:T-Lymphocytes / Q000276:immunology; D013950:Thymus Gland / Q000378:metabolism*; D013967:Thyroiditis, Autoimmune / Q000503:physiopathology*; D014156:Transcortin / Q000378:metabolism*
chemical_list: D005938:Glucocorticoids; D011965:Receptors, Glucocorticoid; D014156:Transcortin; D003345:Corticosterone