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Genetics of type 2 diabetes in European populations.

Abstract Type 2 diabetes (T2D) has become a leading health problem throughout the world. It is caused by environmental and genetic factors, as well as interactions between the two. However, until very recently, the T2D susceptibility genes have been poorly understood. During the past 5 years, with the advent of genome-wide association studies (GWAS), a total of 58 T2D susceptibility loci have been associated with T2D risk at a genome-wide significance level (P < 5 × 10(-8) ), with evidence showing that most of these genetic variants influence pancreatic β-cell function. Most novel T2D susceptibility loci were identified through GWAS in European populations and later confirmed in other ethnic groups. Although the recent discovery of novel T2D susceptibility loci has contributed substantially to our understanding of the pathophysiology of the disease, the clinical utility of these loci in disease prediction and prognosis is limited. More studies using multi-ethnic meta-analysis, gene-environment interaction analysis, sequencing analysis, epigenetic analysis, and functional experiments are needed to identify new susceptibility T2D loci and causal variants, and to establish biological mechanisms.
PMID
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Authors

Mayor MeshTerms

Genome-Wide Association Study

Keywords
Journal Title journal of diabetes
Publication Year Start




PMID- 22781158
OWN - NLM
STAT- MEDLINE
DCOM- 20130201
LR  - 20161019
IS  - 1753-0407 (Electronic)
IS  - 1753-0407 (Linking)
VI  - 4
IP  - 3
DP  - 2012 Sep
TI  - Genetics of type 2 diabetes in European populations.
PG  - 203-12
LID - 10.1111/j.1753-0407.2012.00224.x [doi]
AB  - Type 2 diabetes (T2D) has become a leading health problem throughout the world.
      It is caused by environmental and genetic factors, as well as interactions
      between the two. However, until very recently, the T2D susceptibility genes have 
      been poorly understood. During the past 5 years, with the advent of genome-wide
      association studies (GWAS), a total of 58 T2D susceptibility loci have been
      associated with T2D risk at a genome-wide significance level (P &lt; 5 x 10(-8) ),
      with evidence showing that most of these genetic variants influence pancreatic
      beta-cell function. Most novel T2D susceptibility loci were identified through
      GWAS in European populations and later confirmed in other ethnic groups. Although
      the recent discovery of novel T2D susceptibility loci has contributed
      substantially to our understanding of the pathophysiology of the disease, the
      clinical utility of these loci in disease prediction and prognosis is limited.
      More studies using multi-ethnic meta-analysis, gene-environment interaction
      analysis, sequencing analysis, epigenetic analysis, and functional experiments
      are needed to identify new susceptibility T2D loci and causal variants, and to
      establish biological mechanisms.
CI  - (c) 2012 Ruijin Hospital, Shanghai Jiaotong University School of Medicine and
      Wiley Publishing Asia Pty Ltd.
FAU - Qi, Qibin
AU  - Qi Q
AD  - Department of Nutrition Epidemiology, Harvard School of Public Health, Boston,
      MA, USA.
FAU - Hu, Frank B
AU  - Hu FB
LA  - eng
GR  - R01 DK058845/DK/NIDDK NIH HHS/United States
GR  - DK58845/DK/NIDDK NIH HHS/United States
GR  - P30 DK046200/DK/NIDDK NIH HHS/United States
GR  - U54 CA155626/CA/NCI NIH HHS/United States
GR  - R01 HL071981/HL/NHLBI NIH HHS/United States
GR  - HL071981/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
PL  - Australia
TA  - J Diabetes
JT  - Journal of diabetes
JID - 101504326
SB  - IM
MH  - Asian Continental Ancestry Group/genetics
MH  - China
MH  - Diabetes Mellitus, Type 2/ethnology/*genetics/pathology
MH  - European Continental Ancestry Group/*genetics
MH  - Gene-Environment Interaction
MH  - Genetic Predisposition to Disease/*genetics
MH  - *Genome-Wide Association Study
MH  - Humans
MH  - Prognosis
PMC - PMC3422419
MID - NIHMS391913
EDAT- 2012/07/12 06:00
MHDA- 2013/02/05 06:00
CRDT- 2012/07/12 06:00
PHST- 2012/07/12 06:00 [entrez]
PHST- 2012/07/12 06:00 [pubmed]
PHST- 2013/02/05 06:00 [medline]
AID - 10.1111/j.1753-0407.2012.00224.x [doi]
PST - ppublish
SO  - J Diabetes. 2012 Sep;4(3):203-12. doi: 10.1111/j.1753-0407.2012.00224.x.