title: The GENNID Study. A resource for mapping the genes that cause NIDDM.
abstract: OBJECTIVE
  To develop a resource, consisting of comprehensive data and lymphoblastoid cell lines, of well-characterized NIDDM families that will be available to the scientific community for genetic studies of NIDDM.
  
  
  METHODS
  Non-Hispanic white, Hispanic, African-American, and Japanese-American multiplex NIDDM families, with a minimum of one affected sib-pair, are being collected by the eight Harold Rifkin Family Acquisition Centers. Detailed family and medical histories are obtained from all participants. Family members with diabetes have fasting blood samples drawn, while nondiabetic family members have an oral glucose tolerance test and, when possible, insulin sensitivity and insulin secretion measurements by frequently sampled intravenous glucose tolerance testing or euglycemic insulin clamp. Lymphoblastoid cell lines are established for all participants.
  
  
  RESULTS
  Over 1,400 individuals from approximately 220 families have been studied since the start of the GENNID (Genetics of NIDDM) program in July 1993. The goal is that by July 1997, data from 300 non-Hispanic white families, > 100 Hispanic families, > 100 African-American families, and 15 Japanese-American families will have been collected.
  
  
  CONCLUSIONS
  The identification of the genes responsible for NIDDM may now be achievable, but only if sound phenotypic data are linked to genetic material from a large number of well-described multiplex families. The GENNID project of the American Diabetes Association is creating a comprehensive resource that will expedite the identification of the genetic basis of NIDDM.
authors.affiliation: Cedars-Sinai Research Institute, Los Angeles, California 90048, USA. lraffel@mailgate.csmc.edu
authors.forename: L J
authors.initials: LJ
authors.lastname: Raffel
authors.forename: D C
authors.initials: DC
authors.lastname: Robbins
authors.forename: J M
authors.initials: JM
authors.lastname: Norris
authors.forename: E
authors.initials: E
authors.lastname: Boerwinkle
authors.forename: R A
authors.initials: RA
authors.lastname: DeFronzo
authors.forename: S C
authors.initials: SC
authors.lastname: Elbein
authors.forename: W
authors.initials: W
authors.lastname: Fujimoto
authors.forename: C L
authors.initials: CL
authors.lastname: Hanis
authors.forename: S E
authors.initials: SE
authors.lastname: Kahn
authors.forename: M A
authors.initials: MA
authors.lastname: Permutt
authors.forename: K C
authors.initials: KC
authors.lastname: Chiu
authors.forename: J
authors.initials: J
authors.lastname: Cruz
authors.forename: D A
authors.initials: DA
authors.lastname: Ehrmann
authors.forename: R P
authors.initials: RP
authors.lastname: Robertson
authors.forename: J I
authors.initials: JI
authors.lastname: Rotter
authors.forename: J
authors.initials: J
authors.lastname: Buse
mesh_terms: D001741:Black or African American; D044383:Black People; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D002874:Chromosome Mapping; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000235:genetics*; D005190:Family; D005260:Female; D006630:Hispanic or Latino; D006801:Humans; D007256:Information Systems; D007328:Insulin / Q000097:blood / Q000494:pharmacology; D007564:Japan / Q000208:ethnology; D008055:Lipids / Q000097:blood; D008297:Male; D009679:Nuclear Family; D010375:Pedigree; D010641:Phenotype; D044465:White People
chemical_list: D001786:Blood Glucose; D007328:Insulin; D008055:Lipids