Abstract
Aims/hypothesis: Short and long sleep duration are associated with increased risk of type 2 diabetes. We aimed to investigate whether genetic variants for fasting glucose or type 2 diabetes associate with short or long sleep duration and whether sleep duration modifies the association of genetic variants with these traits. Methods: We examined the cross-sectional relationship between self-reported habitual sleep duration and prevalence of type 2 diabetes in individuals of European descent participating in five studies included in the Candidate Gene Association Resource (CARe), totalling 1,474 cases and 8,323 controls. We tested for association of 16 fasting glucose-associated variants, 27 type 2 diabetes-associated variants and aggregate genetic risk scores with continuous and dichotomised (≤5 h or ≥9 h) sleep duration using regression models adjusted for age, sex and BMI. Finally, we tested whether a gene × behaviour interaction of variants with sleep duration had an impact on fasting glucose or type 2 diabetes risk. Results: Short sleep duration was significantly associated with type 2 diabetes in CARe (OR 1.32; 95% CI 1.08, 1.61; p = 0.008). Variants previously associated with fasting glucose or type 2 diabetes and genetic risk scores were not associated with sleep duration. Furthermore, no study-wide significant interaction was observed between sleep duration and these variants on glycaemic traits. Nominal interactions were observed for sleep duration and PPARG rs1801282, CRY2 rs7943320 and HNF1B rs4430796 in influencing risk of type 2 diabetes (p < 0.05). Conclusions/interpretation: Our findings suggest that differences in habitual sleep duration do not mediate or modify the relationship between common variants underlying glycaemic traits (including in circadian rhythm genes) and diabetes.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 339-346 |
| Number of pages | 8 |
| Journal | Diabetologia |
| Volume | 57 |
| Issue number | 2 |
| DOIs | |
| State | Published - Feb 2014 |
Funding
Funding This study was conducted with support to RS and FAJLS from NIDDK NIH R21 (DK089378) and from Harvard Catalyst of the Harvard Clinical and Translational Science Center (National Center for Research Resources and the National Center for Advancing Translational Sciences, National Institutes of Health Award 8UL1TR000170-05 and financial contributions from Harvard University and its affiliated academic healthcare centres). The content is solely the responsibility of the authors and does not necessarily represent the official views of Harvard Catalyst, Harvard University and its affiliated academic healthcare centres or the National Institutes of Health. CARe and SHHS are supported by the National Heart, Lung, and Blood Institute cooperative agreement U01HL53941 (Boston University), U01HL53916 (University of California, Davis), U01HL53934 (University of Minnesota), U01HL 53937 and U01HL63429 (Johns Hopkins University) and U01HL 63463 (Case Western Reserve University). The CHS was supported by NHLBI contracts HHSN268201200036C, HHSN268200800007C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083 and N01HC85086 and by NHLBI grants HL080295, HL087652 and HL105756, with additional contribution from the National Institute of Neurological Disorders and Stroke (NINDS). Additional support was provided through AG023629 from the National Institute on Aging (NIA). A full list of CHS principal investigators and institutions can be found at www.chs-nhlbi.org/pi.
Keywords
- Circadian genes
- Genetic association studies
- Genetic risk score
- Sleep duration
- Type 2 diabetes
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism
