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Dyslipidemias Among Normoglycemic Members of Familial NIDDM Pedigrees

  1. Mary Catherine Schumacher, MD, MSPH,
  2. Teresa M Maxwell,
  3. Lily L Wu, PHD,
  4. Steven C Hunt, PHD,
  5. Roger R Williams, MD and
  6. Steven C Elbein, MD
  1. Cardiovascular Genetics Research Clinic, Cardiology Division, Department of Internal Medicine, University of Utah School of Medicine Salt Lake City; and the Division of Endocrinology and Metabolism, Department of Internal Medicine, Veterans Affairs Medical Center, and University of Utah School of Medicine Salt Lake City, Utah
  1. Address Correspondence to Dr. Mary C. Schumacher, Cardiovascular Genetics Research Clinic, 410 Chipeta Way, Room 161, Salt Lake City, UT 84108.

Abstract

OBJECTIVE To examine the hypothesis that hyperinsulinemia among relatives of NIDDM probands will increase the prevalence of DLPs, we measured insulin levels and examined the frequency of DLPs among NIDDM pedigree members.

RESEARCH DESIGN AND METHODS We performed 2-h 75-g OGTTs and measured lipid and insulin levels of 287 family members and 86 spouses from 16 large Utah pedigrees ascertained for ≥ 2 siblings with NIDDM.

RESULTS One-hour insulin levels were higher among 206 family members with NGT than among 65 NGT spouses (483.3 vs. 361.7 pM, P = 0.05). Among the NGT family members, 32% had cholesterol levels at or above the age- and sex-specific 90th percentile level defined by the LRC studies, 33% had HDL levels ≤ 10th percentile, and 20% had triglyceride levels ≥ 90th percentile. DLP (any of the three abnormalities) was found among 58% of NGT family members, which was significantly higher than the expected 27% (P < 0.00001) and the prevalence among spouses of 45% (P < 0.05). By NCEP criteria for hyperlipidemia, 40% of family members met criteria for diet and/or pharmacological therapy.

CONCLUSIONS Normoglycemic members of NIDDM pedigrees have a high prevalence of DLPs, which approaches the prevalence in patients with NIDDM. Our data suggest that members of NIDDM pedigrees should be screened carefully for lipid abnormalities.

  • Received January 14, 1991.
  • Accepted January 18, 1992.
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