| Title | Association of genetic predisposition to obesity with type 2 diabetes risk in Han Chinese individuals |
| Authors | Zhu, Jingwen Zong, Geng Lu, Ling Gan, Wei Ji, Linong Hu, Renming Ye, Xingwang Sun, Liang Loos, Ruth J. F. Li, Huaixing Lin, Xu |
| Affiliation | Univ Chinese Acad Sci, Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutrit Sci,Key Lab Nutr & Metab, Shanghai 200031, Peoples R China. Peking Univ, Peoples Hosp, Dept Endocrinol & Metab, Beijing 100871, Peoples R China. Fudan Univ, Shanghai Med Coll, Huashan Hosp, Inst Endocrinol & Diabetol, Shanghai, Peoples R China. Mt Sinai Sch Med, Inst Child Hlth & Dev, Charles Bronfman Inst Personalized Med, Dept Prevent Med,Genet Obesity & Related Traits P, York, NY USA. Univ Chinese Acad Sci, Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutrit Sci,Key Lab Nutr & Metab, 320 Yue Yang Rd, Shanghai 200031, Peoples R China. |
| Keywords | BMI Chinese Genetic risk score HOMA-B Type 2 diabetes BODY-MASS INDEX COMMON VARIANTS LOCI |
| Issue Date | 2014 |
| Publisher | diabetologia |
| Citation | DIABETOLOGIA.2014,57,(9),1830-1833. |
| Abstract | Aims/hypothesis Obesity is a major risk factor for type 2 diabetes, but little is known about the contribution of BMI-associated loci to type 2 diabetes risk in East Asian populations. Methods In this study, 30 known BMI-associated variants and a genetic risk score (GRS) calculated by summing the BMI-increasing alleles of these variants were tested for associations with type 2 diabetes and related glycaemic traits in 1,873 cases of type 2 diabetes and 1,839 controls in Han Chinese individuals. Logistic and linear regression analyses were performed to determine the association with type 2 diabetes risk or related glycaemic traits, respectively, under an additive model with or without adjustment for BMI. Results The GRS was significantly associated with increased BMI (beta [SE] 0.070 [0.016]; p = 1.33 x 10(-5)) in the overall population. Each additional BMI-increasing allele in the GRS increased type 2 diabetes risk by 1.029-fold (95% CI 1.008, 1.050; p = 0.0056) without adjustment for BMI, and the association was slightly attenuated after adjustment for BMI (OR 1.022; 95% CI 1.002, 1.043; p = 0.035). In non-diabetic controls, the GRS was also associated with HOMA of beta cell function (HOMA-B) with adjustment for BMI (beta [SE] -0.876 [0.345]; p = 0.011). Notably, the association of GRS with type 2 diabetes was abolished after adjusting for HOMA-B (OR 1.012; 95% CI 0.986, 1.039; p = 0.380). Conclusions/interpretation Our results suggested that genetic predisposition to obesity leads to increased risk of type 2 diabetes, independent of BMI and partly through impaired beta cell function. |
| URI | http://hdl.handle.net/20.500.11897/209319 |
| ISSN | 0012-186X |
| DOI | 10.1007/s00125-014-3308-7 |
| Indexed | SCI(E) |
| Appears in Collections: | 人民医院 |
