PMID- 28316001
OWN - NLM
STAT- MEDLINE
DCOM- 20171010
LR  - 20221207
IS  - 1573-4978 (Electronic)
IS  - 0301-4851 (Linking)
VI  - 44
IP  - 2
DP  - 2017 Apr
TI  - Associations of polymorphisms in the candidate genes for Alzheimer's disease 
      BIN1, CLU, CR1 and PICALM with gestational diabetes and impaired glucose 
      tolerance.
PG  - 227-231
LID - 10.1007/s11033-017-4100-9 [doi]
AB  - Alzheimer's disease (AD) is the most common type of dementia, with a prevalence 
      that is rising every year. AD is associated with type 2 diabetes mellitus (T2DM) 
      and insulin resistance, and is therefore sometimes called "type 3 diabetes 
      mellitus". The aim of this study was to examine whether the variants of some 
      candidate genes involved in the development of AD, namely BIN1 (rs744373), CLU 
      (rs11136000), CR1 (rs3818361), and PICALM (rs3851179), are related to several 
      disorders of glucose metabolism-gestational diabetes (GDM), T2DM and impaired 
      glucose tolerance (IGT). Our study included 550 women with former GDM and 717 
      control women, 392 patients with T2DM and 180 non-diabetic controls, and 117 
      patients with IGT and 630 controls with normal glucose tolerance. Genotyping 
      analysis was performed using specially-designed TaqMan assays. No significant 
      associations of the genetic variants rs744373 in BIN1, rs11136000 in CLU, or 
      rs3818361 in CR1 were found with GDM, T2DM or IGT, but rs3851179 in PICALM was 
      associated with an increased risk of GDM. The frequency of the AD risk-associated 
      C allele was significantly higher in the GDM group compared to controls: OR 1.21; 
      95% CI (1.03-1.44). This finding was not apparent in T2DM and IGT; conversely, 
      the C allele of the PICALM SNP was protective for IGT: OR 0.67; 95% CI 
      (0.51-0.89). This study demonstrates an association between PICALM rs3851179 and 
      GDM as well as IGT. However, elucidation of the possible role of this gene in the 
      pathogenesis of GDM requires further independent studies.
FAU - Vacinova, Gabriela
AU  - Vacinova G
AD  - Department of Molecular Endocrinology, Institute of Endocrinology, Narodni 8, 
      Prague, 116 94, Czech Republic. gvacinova@endo.cz.
AD  - Department of Anthropology and Human Genetics, Faculty of Science, Charles 
      University in Prague, Prague, Czech Republic. gvacinova@endo.cz.
FAU - Vejrazkova, D
AU  - Vejrazkova D
AD  - Department of Molecular Endocrinology, Institute of Endocrinology, Narodni 8, 
      Prague, 116 94, Czech Republic.
FAU - Lukasova, P
AU  - Lukasova P
AD  - Department of Molecular Endocrinology, Institute of Endocrinology, Narodni 8, 
      Prague, 116 94, Czech Republic.
FAU - Lischkova, O
AU  - Lischkova O
AD  - Department of Molecular Endocrinology, Institute of Endocrinology, Narodni 8, 
      Prague, 116 94, Czech Republic.
FAU - Dvorakova, K
AU  - Dvorakova K
AD  - Department of Molecular Endocrinology, Institute of Endocrinology, Narodni 8, 
      Prague, 116 94, Czech Republic.
FAU - Rusina, R
AU  - Rusina R
AD  - Thomayer Hospital, Prague, Czech Republic.
AD  - Department of Neurology and Center of Clinical Neuroscience, First Faculty of 
      Medicine and General University Hospital in Prague, Charles University in Prague, 
      Prague, Czech Republic.
FAU - Holmerova, I
AU  - Holmerova I
AD  - Faculty of Humanities, Charles University in Prague, Prague, Czech Republic.
FAU - Vankova, H
AU  - Vankova H
AD  - Faculty of Humanities, Charles University in Prague, Prague, Czech Republic.
AD  - Third Faculty of Medicine, Charles University in Prague, Prague, Czech Republic.
FAU - Vcelak, J
AU  - Vcelak J
AD  - Department of Molecular Endocrinology, Institute of Endocrinology, Narodni 8, 
      Prague, 116 94, Czech Republic.
FAU - Bendlova, B
AU  - Bendlova B
AD  - Department of Molecular Endocrinology, Institute of Endocrinology, Narodni 8, 
      Prague, 116 94, Czech Republic.
FAU - Vankova, M
AU  - Vankova M
AD  - Department of Molecular Endocrinology, Institute of Endocrinology, Narodni 8, 
      Prague, 116 94, Czech Republic.
LA  - eng
PT  - Journal Article
DEP - 20170318
PL  - Netherlands
TA  - Mol Biol Rep
JT  - Molecular biology reports
JID - 0403234
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (BIN1 protein, human)
RN  - 0 (CLU protein, human)
RN  - 0 (CR1 protein, human)
RN  - 0 (Clusterin)
RN  - 0 (Monomeric Clathrin Assembly Proteins)
RN  - 0 (Nuclear Proteins)
RN  - 0 (PICALM protein, human)
RN  - 0 (Receptors, Complement 3b)
RN  - 0 (Tumor Suppressor Proteins)
SB  - IM
MH  - Adaptor Proteins, Signal Transducing/blood/genetics
MH  - Adult
MH  - Aged
MH  - Alleles
MH  - Alzheimer Disease/complications/*genetics
MH  - Clusterin/blood/genetics
MH  - Diabetes Mellitus, Type 2/genetics
MH  - Diabetes, Gestational/*genetics/metabolism
MH  - Female
MH  - Gene Frequency
MH  - Genetic Association Studies/methods
MH  - Genetic Predisposition to Disease
MH  - Genetic Variation
MH  - Glucose Intolerance/*genetics/metabolism
MH  - Humans
MH  - Middle Aged
MH  - Monomeric Clathrin Assembly Proteins/blood/*genetics
MH  - Nuclear Proteins/blood/genetics
MH  - Odds Ratio
MH  - Polymorphism, Single Nucleotide/genetics
MH  - Pregnancy
MH  - Receptors, Complement 3b/blood/genetics
MH  - Risk Factors
MH  - Tumor Suppressor Proteins/blood/genetics
MH  - White People/genetics
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - Gestational diabetes mellitus
OT  - Glucose metabolism
OT  - Impaired glucose tolerance
OT  - Polymorphisms
OT  - Type 2 diabetes mellitus
EDAT- 2017/03/21 06:00
MHDA- 2017/10/11 06:00
CRDT- 2017/03/20 06:00
PHST- 2016/02/01 00:00 [received]
PHST- 2017/03/11 00:00 [accepted]
PHST- 2017/03/21 06:00 [pubmed]
PHST- 2017/10/11 06:00 [medline]
PHST- 2017/03/20 06:00 [entrez]
AID - 10.1007/s11033-017-4100-9 [pii]
AID - 10.1007/s11033-017-4100-9 [doi]
PST - ppublish
SO  - Mol Biol Rep. 2017 Apr;44(2):227-231. doi: 10.1007/s11033-017-4100-9. Epub 2017 
      Mar 18.