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

Nathalie Marissal-Arvy, Marie-Neige Campas, Audrey Semont, Céline Ducroix-Crepy, Marie-Christine Beauvieux, Julie Brossaud, Jean-Benoit Corcuff, Jean-Christophe Helbling, Sylvie Vancassel, Anne-Karine Bouzier-Sore, Katia Touyarot, Guillaume Ferreira, Pascal Barat, Marie-Pierre Moisan
Psychoneuroendocrinology. 2018-07-01; 93: 72-81
DOI: 10.1016/j.psyneuen.2018.04.016

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1. Psychoneuroendocrinology. 2018 Jul;93:72-81. doi: 10.1016/j.psyneuen.2018.04.016.
Epub 2018 Apr 17.

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

Marissal-Arvy N(1), Campas MN(2), Semont A(1), Ducroix-Crepy C(1), Beauvieux
MC(3), Brossaud J(1), Corcuff JB(1), Helbling JC(1), Vancassel S(1), Bouzier-Sore
AK(3), Touyarot K(1), Ferreira G(1), Barat P(2), Moisan MP(4).

Author information:
(1)INRA, Univ. Bordeaux, Nutrition and Integrated Neurobiology UMR1286, 146 rue
Leo Saignat, 33076, Bordeaux, France.
(2)INRA, Univ. Bordeaux, Nutrition and Integrated Neurobiology UMR1286, 146 rue
Leo Saignat, 33076, Bordeaux, France; CHU Bordeaux, Unité d’endocrinologie et de
diabétologie pédiatrique, Hôpital des Enfants, Place Amélie Rabat-Léon, 33076,
Bordeaux, France.
(3)CNRS, Univ. Bordeaux, Centre de Résonance Magnétique des Systèmes Biologiques
UMR 5536, 146 rue Leo Saignat, 33076, Bordeaux, France.
(4)INRA, Univ. Bordeaux, Nutrition and Integrated Neurobiology UMR1286, 146 rue
Leo Saignat, 33076, Bordeaux, France. Electronic address:
*protected email*.

The 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 


Auteurs Bordeaux Neurocampus