LAUSR

Purpose Clinical studies suggest that 25-hydroxyvitamin D (25[OH]D) deficiency plays a pivotal role in both type 2 diabetes mellitus (T2DM) and cognitive impairment. However, it is unclear if 25(OH)D deficiency could be a possible cause of cognitive impairment in T2DM. Vitamin-D binding protein (VDBP) acts as a major 25(OH)D transporter. Preclinical study has demonstrated improvement in cognitive function by VDBP via inhibiting synaptic degeneration. The aim of the study was to assess the association between serum 25(OH)D, VDBP and cognitive impairment in T2DM patients. Patients and methods In this case-control study, cognitive function was assessed using the Mini-Mental State Examination (MMSE) and serum 25(OH)D and VDBP levels were estimated using ELISA kits. Results A total of 88 subjects were included in the study. T2DM patients had lower serum 25(OH)D (p=0.02), VDBP levels (p=0.04) and MMSE scores (p<0.0001) than controls. T2DM patients had higher prevalence of 25(OH)D deficiency and insufficiency, aOR 0.322 (0.128–0.809), p=0.016 and cognitive impairment, aOR 4.405 (1.617–12.002); p=0.004. Cognitive impairment was associated with serum 25(OH)D, aOR 0.131 (0.027–0.638); p=0.014 and VDBP, aOR 1.008 (1.001–1.015), p=0.029. A general linear model showed a significant association of MMSE with serum 25(OH)D (p=0.022). Conclusion Serum 25(OH)D deficiency and cognitive impairment was higher in T2DM patients. Routine assessment of cognitive function is suggested to prevent further behavioral complications. The association of VDBP and cognitive impairment in T2DM needs further exploration.