PMID- 23840762
OWN - NLM
STAT- MEDLINE
DCOM- 20140424
LR  - 20221207
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 6
DP  - 2013
TI  - Large scale meta-analyses of fasting plasma glucose raising variants in GCK, 
      GCKR, MTNR1B and G6PC2 and their impacts on type 2 diabetes mellitus risk.
PG  - e67665
LID - 10.1371/journal.pone.0067665 [doi]
LID - e67665
AB  - BACKGROUND: The evidence that the variants GCK rs1799884, GCKR rs780094, MTNR1B 
      rs10830963 and G6PC2 rs560887, which are related to fasting plasma glucose 
      levels, increase the risk of type 2 diabetes mellitus (T2DM) is contradictory. We 
      therefore performed a meta-analysis to derive a more precise estimation of the 
      association between these polymorphisms and T2DM. METHODS: All the publications 
      examining the associations of these variants with risk of T2DM were retrieved 
      from the MEDLINE and EMBASE databases. Using the data from the retrieved 
      articles, we computed summary estimates of the associations of the four variants 
      with T2DM risk. We also examined the studies for heterogeneity, as well as for 
      bias of the publications. RESULTS: A total of 113,025 T2DM patients and 199,997 
      controls from 38 articles were included in the meta-analysis. Overall, the pooled 
      results indicated that GCK (rs1799884), GCKR (rs780094) and MTNR1B (rs10830963) 
      were significantly associated with T2DM susceptibility (OR, 1.04; 95%CI, 
      1.01-1.08; OR, 1.08; 95%CI, 1.05-1.12 and OR, 1.05; 95%CI, 1.02-1.08, 
      respectively). After stratification by ethnicity, significant associations for 
      the GCK, MTNR1B and G6PC2 variants were detected only in Caucasians (OR, 1.09; 
      95%CI, 1.02-1.16; OR, 1.10; 95%CI, 1.08-1.13 and OR, 0.97; 95%CI, 0.95-0.99, 
      respectively), but not in Asians (OR, 1.02, 95% CI 0.98-1.05; OR, 1.01; 95%CI, 
      0.98-1.04 and OR, 1.12; 95%CI, 0.91-1.32, respectively). CONCLUSIONS: Our 
      meta-analyses demonstrated that GCKR rs780094 variant confers high 
      cross-ethnicity risk for the development of T2DM, while significant associations 
      between GCK, MTNR1B and G6PC2 variants and T2DM risk are limited to Caucasians.
FAU - Wang, Haoran
AU  - Wang H
AD  - Department of Internal Medicine, Tongji Hospital, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Liu, Lei
AU  - Liu L
FAU - Zhao, Jinzhao
AU  - Zhao J
FAU - Cui, Guanglin
AU  - Cui G
FAU - Chen, Chen
AU  - Chen C
FAU - Ding, Hu
AU  - Ding H
FAU - Wang, Dao Wen
AU  - Wang DW
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
DEP - 20130628
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Blood Glucose)
RN  - 0 (GCKR protein, human)
RN  - 0 (Germinal Center Kinases)
RN  - 0 (MTNR1B protein, human)
RN  - 0 (Receptor, Melatonin, MT1)
RN  - 0 (Receptor, Melatonin, MT2)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 3.1.3.9 (Glucose-6-Phosphatase)
RN  - EC 3.1.3.9. (G6PC2 protein, human)
SB  - IM
MH  - Adaptor Proteins, Signal Transducing/*genetics/metabolism
MH  - Asian People/genetics
MH  - Blood Glucose/*genetics
MH  - Diabetes Mellitus, Type 2/*genetics/metabolism
MH  - Fasting
MH  - Genetic Predisposition to Disease/genetics
MH  - Germinal Center Kinases
MH  - Glucose-6-Phosphatase/*genetics/metabolism
MH  - Humans
MH  - Polymorphism, Single Nucleotide/*genetics
MH  - Protein Serine-Threonine Kinases/*genetics
MH  - Receptor, Melatonin, MT1/*genetics/metabolism
MH  - Receptor, Melatonin, MT2
MH  - Risk
MH  - White People/genetics
PMC - PMC3695948
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/07/11 06:00
MHDA- 2014/04/25 06:00
PMCR- 2013/06/28
CRDT- 2013/07/11 06:00
PHST- 2013/02/04 00:00 [received]
PHST- 2013/05/22 00:00 [accepted]
PHST- 2013/07/11 06:00 [entrez]
PHST- 2013/07/11 06:00 [pubmed]
PHST- 2014/04/25 06:00 [medline]
PHST- 2013/06/28 00:00 [pmc-release]
AID - PONE-D-13-05066 [pii]
AID - 10.1371/journal.pone.0067665 [doi]
PST - epublish
SO  - PLoS One. 2013 Jun 28;8(6):e67665. doi: 10.1371/journal.pone.0067665. Print 2013.