Linkage of the Metabolic Syndrome to 1q23-q31 in Hispanic Families

The Insulin Resistance Atherosclerosis Study Family Study

  1. Carl D. Langefeld1,
  2. Lynne E. Wagenknecht1,
  3. Jerome I. Rotter2,
  4. Adrienne H. Williams1,
  5. John E. Hokanson3,
  6. Mohammad F. Saad4,
  7. Donald W. Bowden5,
  8. Stephen Haffner6,
  9. Jill M. Norris3,
  10. Stephen S. Rich1 and
  11. Braxton D. Mitchell7
  1. 1Department of Public Health Sciences, Wake Forest University Health Sciences, Winston-Salem, North Carolina
  2. 2Division of Medical Genetics, Cedars-Sinai Medical Center, Los Angeles, California
  3. 3Department of Preventive Medicine, University of Colorado Health Sciences, Denver, Colorado
  4. 4Division of Endocrinology, University of California, Los Angeles, California
  5. 5Department of Biochemistry, Wake Forest University Health Sciences, Winston-Salem, North Carolina
  6. 6Division of Clinical Epidemiology, Department of Medicine, University of Texas Health Science Center, San Antonio, Texas
  7. 7Division of Endocrinology, Diabetes, and Nutrition, University of Maryland School of Medicine, Baltimore, Maryland
  1. Address correspondencereprint requests to Carl D. Langefeld, PhD, Department of Public Health Sciences, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1063. E-mail: clangefe{at}wfubmc.edu

Abstract

The metabolic syndrome is characterized by central obesity, dyslipidemia, elevated blood pressure, and hyperglycemia. The Insulin Resistance Atherosclerosis Study (IRAS) Family Study recruited extended pedigrees of Hispanic descent from San Antonio, TX (SA) and San Luis Valley, CO (SLV). Thirty-five of these pedigrees (27 SA and 8 SLV) had at least 2 individuals with metabolic syndrome (216 affected individuals and 563 affected relative pairs). The prevalence of metabolic syndrome and component criteria in subjects from these pedigrees were 35% metabolic syndrome, 43% increased waist circumference, 31% hypertriglyceridemia, 69% low HDL cholesterol, 31% increased blood pressure, and 25% either increased fasting glucose or presence of diabetes. Nonparametric linkage analysis provided evidence for linkage of metabolic syndrome to 1q23-q31 (D1S518; logarithm of odds [LOD] 1.6) with significant site heterogeneity (SA LOD 2.6 and SLV LOD 0.0), and removing all individuals with diabetes reduced, but did not eliminate, the evidence for linkage to this region (LOD 1.2). This heterogeneity may partially be explained by phenotypic differences. Members in the SA pedigrees were older, had greater central obesity, had higher prevalence of the metabolic syndrome, and were from a more urban environment than members of the SLV pedigrees. These results contribute to the growing evidence that chromosome 1q harbors at least one locus related to the metabolic precursors of diabetes.

Footnotes

    • Accepted January 14, 2004.
    • Received September 16, 2003.
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