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The GENNID Study: A resource for mapping the genes that cause NIDDM

  1. Leslie J Raffel, MD,
  2. David C Robbins, MD,
  3. Jill M Norris, PHD,
  4. Eric Boerwinkle, PHD,
  5. Ralph A DeFronzo, MD,
  6. Steven C Elbein, MD,
  7. Wilfred Fujimoto, MD,
  8. Craig L Hanis, PHD,
  9. Steven E Kahn, MB, CHB,
  10. M Alan Permutt, MD,
  11. Ken C Chiu, MD,
  12. Jaime Cruz, MD, MPH,
  13. David A Ehrmann, MD,
  14. R Paul Robertson, MD,
  15. Jerome I Rotter, MD and
  16. John Buse, MD
  1. Cedars-Sinai Research Institute and University of California Los Angeles California
  2. Medlantic Research Institute Washington, DC
  3. University of Colorado Health Sciences Center Denver, Colorado
  4. University of Texas Health Science Center Houston
  5. University of Texas Health Science Center San Antonio, Texas
  6. Department of Veterans Affairs Medical Center and University of Utah Salt Lake City, Utah
  7. University of Washington Seattle, Washington
  8. Department of Veterans Affairs Medical Center Seattle, Washington
  9. Washington University School of Medicine St. Louis, Missouri
  10. University of Chicago Chicago, Illinois
  11. University of Minnesota Minneapolis, Minnesota
  12. and University of North Carolina School of Medicine Chapel Hill, North Carolina
  1. Address correspondence and reprint requests to Leslie J. Raffel, MD, Associate Director, Common Disease Genetics Program, Division of Medical Genetics, Cedars-Medical Center, 8700 Beverly Blvd., SSB-378, Los Angeles, CA 90048. E-mail: lraffel{at}mailgate.csmc.edu

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.

RESEARCH DESIGN AND 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 ∼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.

  • Received December 11, 1995.
  • Revision received April 18, 1996.
  • Accepted April 18, 1996.
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