title: Genetic variants in potassium channels are associated with type 2 diabetes in a Mongolian population.
abstract: BACKGROUND
  Recent genome-wide association studies (GWAS) have identified more than 40 common sequence variants associated with type 2 diabetes (T2D). However, the results are not always the same in populations with differing genetic backgrounds. In the present study, we evaluated a hypothesis that a North Asian population living in a geographic area with unusually harsh environmental conditions would develop unique genetic risks.
  
  
  METHODS
  A population-based association study was performed with 21 single-nucleotide polymorphisms (SNPs) in nine genes selected according to the results of GWAS conducted in other populations. The study participants included 393 full-heritage Mongolian individuals (177 diagnosed with T2D and 216 matched controls). Genotyping was performed by TaqMan methodology.
  
  
  RESULTS
  The strongest association was detected with SNPs located within the potassium channel-coding genes KCNQ1 (highest odds ratio [OR] = 1.92; P = 3.4 × 10(-5) ) and ABCC8 (OR = 1.79; P = 5 × 10(-4) ). Genetic variants identified as strongly influencing the risk of T2D in other populations (e.g. KCNJ11 or TCF7L2) did not show significant association in Mongolia.
  
  
  CONCLUSIONS
  The strongest T2D risk-associated SNPs in Mongolians are located within two of three tested potassium channel-coding genes. Accumulated variations in these genes may be related to the exposure to harsh environmental conditions.
authors.affiliation: National Institute of Neurological Disorders and Stroke Infectious Diseases and Immunogenetics Section, National Institutes of Health, Bethesda, MD, USA.
authors.forename: Zagaa
authors.initials: Z
authors.lastname: Odgerel
authors.forename: Hee S
authors.initials: HS
authors.lastname: Lee
authors.forename: Narnygerel
authors.initials: N
authors.lastname: Erdenebileg
authors.forename: Suren
authors.initials: S
authors.lastname: Gandbold
authors.forename: Munkhjargal
authors.initials: M
authors.lastname: Luvsanjamba
authors.forename: Nyamkhishig
authors.initials: N
authors.lastname: Sambuughin
authors.forename: Sainbileg
authors.initials: S
authors.lastname: Sonomtseren
authors.forename: Purevdulam
authors.initials: P
authors.lastname: Sharavdorj
authors.forename: Erdenezul
authors.initials: E
authors.lastname: Jodov
authors.forename: Khasag
authors.initials: K
authors.lastname: Altaisaikhan
authors.forename: Lev G
authors.initials: LG
authors.lastname: Goldfarb
mesh_terms: D018528:ATP-Binding Cassette Transporters / Q000235:genetics; D000483:Alleles; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics*; D005787:Gene Frequency; D059647:Gene-Environment Interaction; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D055106:Genome-Wide Association Study; D005838:Genotype; D006801:Humans; D007438:Introns / Q000235:genetics; D051657:KCNQ1 Potassium Channel / Q000235:genetics*; D015810:Linkage Disequilibrium; D008875:Middle Aged; D008986:Mongolia; D020641:Polymorphism, Single Nucleotide; D024661:Potassium Channels, Inwardly Rectifying / Q000235:genetics; D011955:Receptors, Drug / Q000235:genetics; D012307:Risk Factors; D064233:Sulfonylurea Receptors
chemical_list: D018528:ATP-Binding Cassette Transporters; D051657:KCNQ1 Potassium Channel; C496909:KCNQ1 protein, human; D024661:Potassium Channels, Inwardly Rectifying; D011955:Receptors, Drug; D064233:Sulfonylurea Receptors