Effect of vitamin D3 on behavioural and biochemical parameters in diabetes type 1-induced rats

• Published in: Cell biochemistry and function Vol. 32; no. 6; pp. 502 - 510
• Main Authors: Calgaroto, Nicéia Spanholi, Thomé, Gustavo Roberto, da Costa, Pauline, Baldissareli, Jucimara, Hussein, Fátima Abdala, Schmatz, Roberta, Rubin, Maribel A., Signor, Cristiane, Ribeiro, Daniela Aymone, Carvalho, Fabiano Barbosa, de Oliveira, Lizielle Souza, Pereira, Luciane Belmonte, Morsch, Vera Maria, Schetinger, Maria Rosa Chitolina
• Format: Journal Article
• Language: English
• Published: England Blackwell Publishing Ltd 01.08.2014; Wiley Subscription Services, Inc
• Subjects: Acetylcholinesterase - metabolism; Animals; Blood Glucose - drug effects; Body Weight - drug effects; Cerebral Cortex - drug effects; cholecalciferol; Cholecalciferol - pharmacology; Cholecalciferol - therapeutic use; cholinesterase; diabetes; Diabetes Mellitus, Type 1 - chemically induced; Diabetes Mellitus, Type 1 - drug therapy; Diabetes Mellitus, Type 1 - metabolism; Diabetes Mellitus, Type 1 - psychology; Eating - drug effects; Fear - drug effects; Hypoglycemic Agents - pharmacology; Male; memory; Memory - drug effects; Metformin - pharmacology; Porphobilinogen Synthase - metabolism; Rats, Wistar; Sodium-Potassium-Exchanging ATPase - metabolism; Streptozocin; Thiobarbituric Acid Reactive Substances - metabolism; VD3; Vitamins - pharmacology; Vitamins - therapeutic use; cholecalciferol; memory; VD3; cholinesterase; diabetes
• ISSN: 0263-6484; 1099-0844
• DOI: 10.1002/cbf.3044

Diabetes is associated with long‐term complications in the brain and reduced cognitive ability. Vitamin D3 (VD3) appears to be involved in the amelioration of hyperglycaemia in streptozotocin (STZ)‐induced diabetic rats. Our aim was to analyse the potential of VD3 in avoiding brain damage through evaluation of acetylcholinesterase (AChE), Na+K+‐adenosine triphosphatase (ATPase) and delta aminolevulinate dehydratase (δ‐ALA‐D) activities and thiobarbituric acid reactive substance (TBARS) levels from cerebral cortex, as well as memory in STZ‐induced diabetic rats. Animals were divided into eight groups (n = 5): control/saline, control/metformin (Metf), control/VD3, control/Metf + VD3, diabetic/saline, diabetic/Metf, diabetic/VD3 and diabetic/Metf + VD3. Thirty days after treatment, animals were submitted to contextual fear‐conditioning and open‐field behavioural tests, after which they were sacrificed and the cerebral cortex was dissected. Our results demonstrate a significant memory deficit, an increase in AChE activity and TBARS levels and a decrease in δ‐ALA‐D and Na+K+‐ATPase activities in diabetic rats when compared with the controls. Treatment of diabetic rats with Metf and VD3 prevented the increase in AChE activity when compared with the diabetic/saline group. In treated diabetic rats, the decrease in Na+K+‐ATPase was reverted when compared with non‐treated rats, but the increase in δ‐ALA‐D activity was not. VD3 prevented diabetes‐induced TBARS level and improved memory. Our results show that VD3 can avoid cognitive deficit through prevention of changes in important enzymes such as Na+K+‐ATPase and AChE in cerebral cortex in type 1 diabetic rats. Copyright © 2014 John Wiley & Sons, Ltd.