title: Vitamin A regulates hypothalamic-pituitary-adrenal axis status in LOU/C rats.
abstract: The aim of this study was to explore the involvement of retinoids in the hypoactivity and hyporeactivity to stress of the hypothalamic-pituitary-adrenal (HPA) axis in LOU/C rats. We measured the effects of vitamin A deficiency administered or not with retinoic acid (RA) on plasma corticosterone in standard conditions and in response to restraint stress and on hypothalamic and hippocampal expression of corticosteroid receptors, corticotropin-releasing hormone and 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) in LOU/C rats. Interestingly, under control conditions, we measured a higher plasma concentration of retinol in LOU/C than in Wistar rats, which could contribute to the lower basal activity of the HPA axis in LOU/C rats. Vitamin A deficiency induced an increased HPA axis activity in LOU/C rats, normalized by RA administration. Compared with LOU/C control rats, vitamin A-deficient rats showed a delayed and heightened corticosterone response to restraint stress. The expression of corticosteroid receptors was strongly decreased by vitamin A deficiency in the hippocampus, which could contribute to a less efficient feedback by corticosterone on HPA axis tone. The expression of 11β-HSD1 was increased by vitamin A deficiency in the hypothalamus (+62.5%) as in the hippocampus (+104.7%), which could lead to a higher production of corticosterone locally and contribute to alteration of the hippocampus. RA supplementation treatment restored corticosterone concentrations and 11β-HSD1 expression to control levels. The high vitamin A status of LOU/C rats could contribute to their low HPA axis activity/reactivity and to a protective effect against 11β-HSD1-mediated deleterious action on cognitive performances during ageing.
authors.affiliation: INRA, Nutrition and Integrative Neurobiology, UMR1286, Université de Bordeaux 2, 146, rue Léo Saignat, 33076 Bordeaux Cedex, France.
authors.forename: Nathalie
authors.initials: N
authors.lastname: Marissal-Arvy
authors.forename: Rachel
authors.initials: R
authors.lastname: Hamiani
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Richard
authors.forename: Marie-Pierre
authors.initials: MP
authors.lastname: Moisan
authors.forename: Véronique
authors.initials: V
authors.lastname: Pallet
mesh_terms: D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1 / Q000096:biosynthesis; D000818:Animals; D003345:Corticosterone / Q000097:blood; D003346:Corticotropin-Releasing Hormone / Q000096:biosynthesis; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects* / Q000502:physiology; D008297:Male; D010913:Pituitary-Adrenal System / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D017208:Rats, Wistar; D013312:Stress, Physiological; D013315:Stress, Psychological / Q000503:physiopathology; D014212:Tretinoin / Q000627:therapeutic use; D014801:Vitamin A / Q000097:blood / Q000494:pharmacology*; D014802:Vitamin A Deficiency / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology
chemical_list: D014801:Vitamin A; D014212:Tretinoin; D003346:Corticotropin-Releasing Hormone; D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1; D003345:Corticosterone
keywords: LOU/C; glucocorticoid; rat; retinol; stress