One small step for mice, one giant leap for GWAS?
Mark A. Herman,1,2 Jonathan E. Campbell,1,2 and David A. D’Alessio1
1Duke Molecular Physiology Institute, Department of Medicine, Division of Endocrinology,
2Department of Pharmacology and Cancer Biology, Duke University, Durham, North Carolina, USA.
Address correspondence to: David D’Alessio, 300 N. Duke Street, Duke Molecular Physiology Institute, Division of Endocrinology, Duke University, Durham, North Carolina 27701, USA. Phone: 919.684.5778; Email: david.d’alessio@duke.edu.
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1Duke Molecular Physiology Institute, Department of Medicine, Division of Endocrinology,
2Department of Pharmacology and Cancer Biology, Duke University, Durham, North Carolina, USA.
Address correspondence to: David D’Alessio, 300 N. Duke Street, Duke Molecular Physiology Institute, Division of Endocrinology, Duke University, Durham, North Carolina 27701, USA. Phone: 919.684.5778; Email: david.d’alessio@duke.edu.
Find articles by Campbell, J. in: JCI | PubMed | Google Scholar
1Duke Molecular Physiology Institute, Department of Medicine, Division of Endocrinology,
2Department of Pharmacology and Cancer Biology, Duke University, Durham, North Carolina, USA.
Address correspondence to: David D’Alessio, 300 N. Duke Street, Duke Molecular Physiology Institute, Division of Endocrinology, Duke University, Durham, North Carolina 27701, USA. Phone: 919.684.5778; Email: david.d’alessio@duke.edu.
Find articles by D’Alessio, D. in: JCI | PubMed | Google Scholar
First published September 9, 2019 - More info
© 2019 American Society for Clinical Investigation
Genome-wide association studies (GWAS) have provided a wealth of information on potential disease-associated genes in the human population. In particular, several loci have been associated with type 2 diabetes (T2D). However, due to the complexity of the disease, it has been a challenge to unravel the exact effects of specific loci on T2D pathogenesis. In this issue of the JCI, Keller and colleagues developed a systems genetic approach to identify insulin secretion–associated genes in nondiabetic mice followed by tissue-level and functional phenotyping. Several of the loci identified were syntenic with human T2D-related loci, indicating that this approach may be feasible for discerning genetic variation in nondiabetic individuals that may lead to the development of T2D.
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ISSN: 0021-9738 (print), 1558-8238 (online)