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Cited by 254Genetic Associations and EpidemiologyDiabetes and associated disordersPancreatic function and diabetes

The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.

Type 2 diabetes: new genes, new understanding

Open access
Prokopenko, Inga, McCarthy, Mark I., Lindgren, Cecilia M.·2008·Trends in Genetics
DOI 10.1016/j.tig.2008.09.004PMC PMC7116807
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Abstract

Over the past two years, there has been a spectacular change in the capacity to identify common genetic variants that contribute to predisposition to complex multifactorial phenotypes such as type 2 diabetes (T2D). The principal advance has been the ability to undertake surveys of genome-wide association in large study samples. Through these and related efforts, approximately 20 common variants are now robustly implicated in T2D susceptibility. Current developments, for example in high-throughput resequencing, should help to provide a more comprehensive view of T2D susceptibility in the near future. Although additional investigation is needed to define the causal variants within these novel T2D-susceptibility regions, to understand disease mechanisms and to effect clinical translation, these findings are already highlighting the predominant contribution of defects in pancreatic beta-cell function to the development of T2D.

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  • A polymorphism in KCNJ15 (encoding Kir4.2) increases the risk of T2DM more than 1.7-fold.

    “In addition, a polymorphism in KCNJ15 (the gene encoding Kir4.2) increases the risk of T2DM >1.7-fold (522).”

    From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [522]

    The section “A leap forward in complex trait genetics” discusses KCNJ11 and a 15–20% increase in T2D risk per susceptibility allele, not KCNJ15 or Kir4.2. Searches for KCNJ15, Kir4.2, and a greater-than-1.7-fold risk found no passage in our copy addressing the claimed association. (LLM, conf=0.76)

    Experimental — accuracy not yet measured

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Metadata

Authors
Prokopenko, I., McCarthy, M. I., & Lindgren, C. M.
Affiliations
Centre for Human Genetics (GB)
Corresponding author
McCarthy, Mark I.
ORCID
Venue
Trends in Genetics
Publisher
Elsevier BV
Published
2008-12
Volume
24
Issue
12
Pages
613-621
ISSN
0168-9525 (ISSN-L)
DOI
10.1016/j.tig.2008.09.004
PMC
PMC7116807
OpenAlex
W2005493813
Cited by
254
References
23
Citations by year
2026: 1 · 2025: 2 · 2024: 1 · 2023: 1 · 2022: 5 · 2021: 7 · 2020: 2 · 2019: 6 · 2018: 9 · 2017: 10 · 2016: 12 · 2015: 19 · 2014: 15 · 2013: 28 · 2012: 22
FWCI
3.65
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Trends in Genetics (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • Zenodo (CERN European Organization for Nuclear Research) (submittedVersion, other-oa)
Funders
Wellcome Trust
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Keywords
type 2 diabetes, genetic susceptibility, genome-wide association study, common genetic variants, beta-cell function, complex diseases
MeSH terms
Chromosome Mapping, Diabetes Mellitus, Type 2, Humans, Meta-Analysis as Topic, Quantitative Trait, Heritable, Genetic Predisposition to Disease, Genome-Wide Association Study

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