| Literature DB >> 30718926 |
Yoichiro Kamatani1,2, Momoko Horikoshi3, Ken Suzuki4,5,6,7, Masato Akiyama5,8, Kazuyoshi Ishigaki5, Masahiro Kanai5,9, Jun Hosoe4, Nobuhiro Shojima4, Atsushi Hozawa10,11, Aya Kadota12,13, Kiyonori Kuriki14, Mariko Naito15,16, Kozo Tanno17,18, Yasushi Ishigaki19,20, Makoto Hirata21, Koichi Matsuda22, Nakao Iwata23, Masashi Ikeda23, Norie Sawada24, Taiki Yamaji24, Motoki Iwasaki24, Shiro Ikegawa25, Shiro Maeda6,26,27, Yoshinori Murakami28, Kenji Wakai15, Shoichiro Tsugane29, Makoto Sasaki30,31, Masayuki Yamamoto10,11, Yukinori Okada5,7,32, Michiaki Kubo33, Toshimasa Yamauchi34, Takashi Kadowaki35,36,37.
Abstract
To understand the genetics of type 2 diabetes in people of Japanese ancestry, we conducted A meta-analysis of four genome-wide association studies (GWAS; 36,614 cases and 155,150 controls of Japanese ancestry). We identified 88 type 2 diabetes-associated loci (P < 5.0 × 10-8) with 115 independent signals (P < 5.0 × 10-6), of which 28 loci with 30 signals were novel. Twenty-eight missense variants were in linkage disequilibrium (r2 > 0.6) with the lead variants. Among the 28 missense variants, three previously unreported variants had distinct minor allele frequency (MAF) spectra between people of Japanese and European ancestry (MAFJPN > 0.05 versus MAFEUR < 0.01), including missense variants in genes related to pancreatic acinar cells (GP2) and insulin secretion (GLP1R). Transethnic comparisons of the molecular pathways identified from the GWAS results highlight both ethnically shared and heterogeneous effects of a series of pathways on type 2 diabetes (for example, monogenic diabetes and beta cells).Entities:
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Year: 2019 PMID： 30718926 DOI： 10.1038/s41588-018-0332-4
Source DB: PubMed Journal: Nat Genet ISSN： 1061-4036 Impact factor: 38.330