ABSTRACT
Background: It is common for patients with type 2 diabetes mellitus (T2DM) to have vitamin D deficiency. Aim of the study is to determine the metabolic effects of oral vitamin D supplementation in a cohort of T2DM subjects.Methods: Subjects with T2DM were divided into two groups. Group A (Control) included subjects who received the standard treatment (conventional antidiabetic drugs). Group B (Intervention), apart from the standard treatment (conventional antidiabetic drugs), was also supplemented with Vitamin D3. All the patients were followed up at baseline, 6 months, 12 months and 18 months.Results: Vitamin D deficiency was noted down in all the study subjects. Even after 18 months of supplementation, all subjects remained vitamin D deficient. There was a significant improvement in the circulating levels of 25-hydroxyvitamin D. Improvement in the lipid profile of subjects was observed as evidenced by a decrease in total cholesterol (5.0±0.92 mmol/l) as compared to baseline (5.5±1.6 mmol/l). HOMA-IR changed significantly after 18 months of supplementation from baseline (7.0±1.06 vs 10.8±1.96 nmol/l).Conclusions: Supplementation to achieve higher levels of vitamin D remains a promising adjuvant therapy for T2DM patients. Additionally, the intervention brought out a favourable change in HDL/LDL ratio among study subjects.
ABSTRACT
Background: Understanding the processes underlying cognitive functions is a prerequisite to develop strategies for the treatment of cognitive deficits. There is a great need for valid animal models for investigating the cognitive enhancing effects of potential therapeutics. Many studies have investigated animal models of cognitive deficits by using animals treated with compounds that compromise cognitive abilities. Glutamate, an excitatory neurotransmitter and abundantly distributed in the central nervous system is involved in memory processes through N-methyl-d-aspartate (NMDA) receptors. The behavioural consequences of blocking the NMDA receptor provide the rationale for cognitive impairment as an animal model for the cognitive deficits associated with dementia. Authors investigated the effect of dizocilpine (MK-801), an NMDA-receptor antagonist (non-competitive) on the working memory in rats using the three-panel runway apparatus.Methods: Total 24 trained male albino rats were randomly divided into 4 groups of 6 animals each. Varying doses of MK-801 were administered to the animals. Working memory errors and latency periods were evaluated on the three panel Runway apparatus.Results: Treatment with MK-801 at the dose of 0.03mg/ kg did not result in any significant change in working memory errors or latency period in comparison to saline control. MK-801 treatment at dose of 0.1mg/kg and 0.3mg/kg resulted in a significant increase in the number of working memory errors and latency period as compared to control.Conclusions: Authors conclude that MK-801 treatment in the dose of 0.1mg/ kg and 0.3mg/kg resulted in working memory deficits on the three-panel runway apparatus. Rats with cognitive deficits induced by the prototypical N-methyl-d-aspartate (NMDA) receptor antagonist MK-801 may provide a relevant animal model of dementia based on the mechanistic approach of blocking NMDA/glutamatergic signalling.