Search: onr:"swepub:oai:lup.lub.lu.se:7fd08be3-041e-4222-96c7-8638e41333f9" >
Variation in maturi...
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Billings, Liana K.Harvard Medical School,Massachusetts General Hospital,NorthShore University HealthSystem
(author)
Variation in maturity-onset diabetes of the young genes influence response to interventions for diabetes prevention
- Article/chapterEnglish2017
Publisher, publication year, extent ...
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2017-04-27
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The Endocrine Society,2017
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12 s.
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LIBRIS-ID:oai:lup.lub.lu.se:7fd08be3-041e-4222-96c7-8638e41333f9
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https://lup.lub.lu.se/record/7fd08be3-041e-4222-96c7-8638e41333f9URI
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https://doi.org/10.1210/jc.2016-3429DOI
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Language:English
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Summary in:English
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Subject category:art swepub-publicationtype
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Subject category:ref swepub-contenttype
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Context: Variation in genes that cause maturity-onset diabetes of the young (MODY) has been associated with diabetes incidence and glycemic traits. Objectives: This study aimed to determine whether genetic variation in MODY genes leads to differential responses to insulin-sensitizing interventions. Design and Setting: This was a secondary analysis of a multicenter, randomized clinical trial, the Diabetes Prevention Program (DPP), involving 27 US academic institutions. We genotyped 22 missense and 221 common variants in the MODY-causing genes in the participants in the DPP. Participants and Interventions: The study included 2806 genotyped DPP participants randomized to receive intensive lifestyle intervention (n = 935), metformin (n = 927), or placebo (n = 944). Main Outcome Measures: Association of MODY genetic variants with diabetes incidence at a median of 3 years and measures of 1-year β-Cell function, insulinogenic index, and oral disposition index. Analyses were stratified by treatment group for significant single-nucleotide polymorphism 3 treatment interaction (Pint, 0.05). Sequence kernel association tests examined the association between an aggregate of rare missense variants and insulinogenic traits. Results: After 1 year, the minor allele of rs3212185 (HNF4A) was associated with improved β-Cell function in the metformin and lifestyle groups but not the placebo group; the minor allele of rs6719578 (NEUROD1) was associated with an increase in insulin secretion in the metformin group but not in the placebo and lifestyle groups. Conclusions: These results provide evidence that genetic variation among MODY genes may influence response to insulin-sensitizing interventions.
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Jablonski, Kathleen AGeorge Washington University
(author)
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Warner, A. SofiaMassachusetts General Hospital
(author)
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Cheng, Yu ChienNorthShore University HealthSystem,University of Chicago
(author)
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McAteer, Jarred B.Massachusetts General Hospital
(author)
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Tipton, LauraGeorge Washington University
(author)
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Shuldiner, Alan R.
(author)
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Ehrmann, David AUniversity of Chicago
(author)
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Manning, Alisa K.Broad Institute,Harvard Medical School,Massachusetts General Hospital
(author)
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Dabelea, DanaColorado School of Public Health
(author)
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Franks, Paul W.Lund University,Lunds universitet,Genetisk och molekylär epidemiologi,Forskargrupper vid Lunds universitet,Genetic and Molecular Epidemiology,Lund University Research Groups(Swepub:lu)med-plf
(author)
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Kahn, Steven EUniversity of Washington
(author)
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Pollin, Toni IUniversity of Maryland, Baltimore
(author)
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Knowler, William CNational Institute of Diabetes and Digestive and Kidney Diseases
(author)
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Altshuler, DavidHarvard Medical School,Broad Institute
(author)
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Florez, Jose C.Massachusetts General Hospital,Harvard Medical School,George Washington University,Broad Institute
(author)
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Harvard Medical SchoolMassachusetts General Hospital
(creator_code:org_t)
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Diabetes Prevention Program Research Group
Related titles
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In:Journal of Clinical Endocrinology and Metabolism: The Endocrine Society102:8, s. 2678-26890021-972X1945-7197
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Billings, Liana ...
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Jablonski, Kathl ...
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Warner, A. Sofia
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Cheng, Yu Chien
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McAteer, Jarred ...
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Tipton, Laura
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Shuldiner, Alan ...
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Ehrmann, David A
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Manning, Alisa K ...
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Dabelea, Dana
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Franks, Paul W.
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Kahn, Steven E
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Pollin, Toni I
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Knowler, William ...
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Altshuler, David
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Florez, Jose C.
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