PMID- 31571953
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220410
IS  - 1178-7007 (Print)
IS  - 1178-7007 (Electronic)
IS  - 1178-7007 (Linking)
VI  - 12
DP  - 2019
TI  - Attenuated serum 25-hydroxyvitamin D and vitamin D binding protein associated 
      with cognitive impairment in patients with type 2 diabetes.
PG  - 1763-1772
LID - 10.2147/DMSO.S207728 [doi]
AB  - 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.
CI  - (c) 2019 Parveen et al.
FAU - Parveen, Rizwana
AU  - Parveen R
AD  - Department of Pharmaceutical Medicine, School of Pharmaceutical Education and 
      Research, Jamia Hamdard, New Delhi 110062, India.
FAU - Kapur, Prem
AU  - Kapur P
AD  - Hamdard Institute of Medical Sciences and Research, HAH Centenary Hospital, Jamia 
      Hamdard, New Delhi 110062, India.
FAU - Venkatesh, Shubhashree
AU  - Venkatesh S
AD  - Centre for Translational and Clinical Research, School of Chemical & Life 
      Sciences, Jamia Hamdard, New Delhi 110062, India.
FAU - Agarwal, Nidhi Bharal
AU  - Agarwal NB
AD  - Centre for Translational and Clinical Research, School of Chemical & Life 
      Sciences, Jamia Hamdard, New Delhi 110062, India.
LA  - eng
PT  - Journal Article
DEP - 20190909
PL  - New Zealand
TA  - Diabetes Metab Syndr Obes
JT  - Diabetes, metabolic syndrome and obesity : targets and therapy
JID - 101515585
PMC - PMC6748038
OTO - NOTNLM
OT  - Mini-Mental State Examination
OT  - cognitive dysfunction
OT  - hypovitaminosis D
OT  - vitamin-D insufficiency
COIS- The authors report no conflicts of interest in this work.
EDAT- 2019/10/02 06:00
MHDA- 2019/10/02 06:01
PMCR- 2019/09/09
CRDT- 2019/10/02 06:00
PHST- 2019/03/05 00:00 [received]
PHST- 2019/05/10 00:00 [accepted]
PHST- 2019/10/02 06:00 [entrez]
PHST- 2019/10/02 06:00 [pubmed]
PHST- 2019/10/02 06:01 [medline]
PHST- 2019/09/09 00:00 [pmc-release]
AID - 207728 [pii]
AID - 10.2147/DMSO.S207728 [doi]
PST - epublish
SO  - Diabetes Metab Syndr Obes. 2019 Sep 9;12:1763-1772. doi: 10.2147/DMSO.S207728. 
      eCollection 2019.