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Insulin treatment partially prevents cognitive and hippocampal alterations as well as glucocorticoid dysregulation in early-onset insulin-deficient diabetic rats

hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorMARISSAL-ARVY, Nathalie
dc.contributor.authorCAMPAS, Marie-Neige
hal.structure.identifierInstitut de rythmologie et modélisation cardiaque [Pessac] [IHU Liryc]
dc.contributor.authorSEMONT, Audrey
dc.contributor.authorDUCROIX-CREPY, Celine
hal.structure.identifierBiochimie
dc.contributor.authorBEAUVIEUX, Marie Christine
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorBROSSAUD, Julie
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorCORCUFF, Jean-Benoit
dc.contributor.authorHELBLING, Jean Christophe
hal.structure.identifierNutrition et Régulation Lipidique des Fonctions Cérébrales
dc.contributor.authorVANCASSEL, Sylvie
hal.structure.identifierCentre de résonance magnétique des systèmes biologiques [CRMSB]
dc.contributor.authorBOUZIER-SORE, Anne-Karine
dc.contributor.authorTOUYAROT, Katia
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorFERREIRA, Guillaume
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorBARAT, Pascal
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorMOISAN, Marie Pierre
IDREF: 060242264
dc.date.accessioned2021-10-07T16:29:54Z
dc.date.available2021-10-07T16:29:54Z
dc.date.issued2018-07
dc.identifier.issn0306-4530
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/112674
dc.description.abstractEnThe diagnosis of Type 1 Diabetes (T1D) in ever younger children led us to question the impact of insulin deficiency or chronic hyperglycemia on cerebral development and memory performances. Here, we sought abnormalities in these traits in a model of streptozotocin-induced diabetes in juvenile rats treated or not by insulin. We made the assumption that such alterations would be related, at least in part, to excessive glucocorticoid exposition in hippocampal neurons. We have compared 3 groups of juvenile rats: controls, untreated diabetics and insulin-treated diabetics. Diabetes was induced by streptozotocin (65 mg/kg IP/day, 2 consecutive days), at postnatal days 21 and 22 and a subcutaneous pellet delivering 2 U of insulin/day was implanted in treated diabetic rats 3 days later. Three weeks after diabetes induction, cognitive performances (Y maze, object location and recognition tests), in vivo brain structure (brain volume and water diffusion by structural magnetic resonance imaging), and hippocampal neurogenesis (immunohistochemical labeling) measurements were undertaken. Corticosterone levels were evaluated in plasma under basal and stress conditions, and within hippocampus together with 11β-dehydrocorticosterone to assess 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) activity. The comparison of the three experimental groups revealed that, compared to controls, untreated diabetic rats showed decreased cognitive performances in Y-maze and object location test (p < 0.05), decreased brain and hippocampal microstructure (p < 0.05), and decreased maturation and survival of hippocampal newborn neurons (p < 0.05). These alterations were associated with increased plasma corticosterone at the baseline nadir of its secretion (p < 0.001) and during the recovery phase following a restraint stress (p < 0.001), as well as increased hippocampal corticosterone levels (p < 0.01) and 11β-HSD1 activity (p < 0.05). As untreated diabetic rats, insulin-treated diabetic rats displayed decreased brain volume and water diffusion (p < 0.05 compared to controls) and intermediate memory performances and hippocampal neurogenesis (p value not significant compared to either controls or untreated diabetics). Moreover, they were similar to controls for basal plasma and hippocampal corticosterone and 11β-HSD1 activity but show increased plasma corticosterone during the recovery phase following a restraint stress similar to untreated diabetics (p < 0.001 compared to controls). Thus, insulin did not completely prevent several hippocampal-dependent behavioral and structural alterations induced by diabetes in juvenile rats which may relate to the higher cognitive difficulties encountered in T1D children compared to non-diabetic controls. Although insulin restored basal corticosterone and 11β-HSD1 activity (in hippocampus and plasma), the negative feedback regulation of corticosterone secretion after stress was still impaired in insulin-treated diabetic rats. Further characterization of insulin control on glucocorticoid regulation and availability within hippocampus is awaited.
dc.language.isoen
dc.publisherElsevier
dc.subject11β-Hydroxysteroid dehydrogenase type 1
dc.subjectCorticosterone
dc.subject.enType 1 diabetes
dc.subject.enMemory
dc.subject.enHippocampus
dc.subject.enChildren
dc.title.enInsulin treatment partially prevents cognitive and hippocampal alterations as well as glucocorticoid dysregulation in early-onset insulin-deficient diabetic rats
dc.typeArticle de revue
dc.identifier.doi10.1016/j.psyneuen.2018.04.016
dc.subject.halSciences du Vivant [q-bio]
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]
bordeaux.journalPsychoneuroendocrinology
bordeaux.page72-81
bordeaux.volume93
bordeaux.hal.laboratoriesCentre de Résonance Magnétique des Systèmes Biologiques (CRMSB) - UMR 5536*
bordeaux.issue144
bordeaux.institutionUniversité de Bordeaux
bordeaux.institutionCNRS
bordeaux.institutionINRAE
bordeaux.peerReviewedoui
hal.identifierhal-02348253
hal.version1
hal.origin.linkhttps://hal.archives-ouvertes.fr//hal-02348253v1
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