Effect of vitamin D₃on behavioural and biochemical parameters in diabetes type 1‐induced rats

Abstract

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.

TLR2 knockout protects against diabetes-mediated changes in cerebral perfusion and cognitive deficits

“…One method of testing long-term hippocampus and prefrontal cortex-dependent learning that does not depend on locomotor activity for assessment is fear-conditioned learning. STZinduced diabetes has been shown to lead a reduction in longterm hippocampus-dependent fear learning assessed during contextual fear-conditioning testing (6). We similarly observed impairment in long-term hippocampus-dependent learning at 24 h, as well as impaired prefrontal cortex-dependent learning at 4 and 14 days in the diabetic WT STZ mice.…”

Serum 1, 25-Hydroxyvitamin D: A Useful Index of Cognitive and Physical Functional Impairment in Healthy Older Adults in Japan: A Pilot Study

“…Skeletal muscle mitochondrial function declines and oxidative stress increases with advancing age [19], and these changes have been implicated in the etiology of sarcopenia [20]. 1, 25OHD was re-ported to have a significant physiological antioxidant activity [21]. Thus 1, 25OHD passively acts by activation of the antioxidant pathway.…”

Vitamin D3 Supplementation Improved Cognitive Function in Diabetic Elderly Patients with Good Glycemic Control in Japan: A Pilot Study

“…Over expression of reactive oxygen species (ROS) stimulated by disruption of cerebral blood flow was shown to be one of the main causes of vascular dementia-induced cognitive deficits in a rat model [20]. 1, 25OHD was reported to have significant physiological antioxidant activity [21]. These results suggest a potential role of vitamin D in treating patients with cognitive dysfunction in DM.…”