J E McCarthy

University of California, Los Angeles, Los Angeles, CA, United States

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Publications (2)5.38 Total impact

  • K C Chiu, J E McCarthy
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    ABSTRACT: Plasma angiotensin I-converting enzyme (ACE) levels are genetically predetermined and are correlated with a deletion (D) insertion (I) polymorphism at the ACE gene locus. A subset of diabetic patients are noted to have elevated ACE levels. Treatment with ACE inhibitors has been shown to improve insulin sensitivity in both diabetic and nondiabetic subjects. We examined the relationship of D/I polymorphism and insulin sensitivity in 24 glucose-tolerant subjects by an oral glucose tolerance test (OGTT) and glucose clamps. Subjects with the I allele had higher insulin levels at 90 minutes (515 +/- 69 v 250 +/- 43 pmol/L, P = .008) and higher insulin area under the curve (56,200 +/- 8,148 v 33,300 +/- 8,114, P = .022) after glucose challenge compared with subjects without the I allele. During the euglycemic clamp, subjects with the I allele require less glucose infusion to maintain euglycemia than subjects without the I allele (5.343 +/- 0.743 v 8.944 +/- 1.272 mg/kg/min, P = .020). We conclude that the I allele is associated with insulin resistance in glucose-tolerant and normotensive African-Americans.
    Metabolism 05/1997; 46(4):395-9. · 3.10 Impact Factor
  • K C Chiu, J E McCarthy
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    ABSTRACT: We have previously reported a common variation in the liver promoter of the human glucokinase, which is regulated by insulin, in the patients with non-insulin-dependent diabetes mellitus (NIDDM). The variation occurred within a 10-bp region completely conserved between human and rat. Its basic motif was almost identical to the insulin regulatory element of the phosphoenolpyruvate carboxykinase gene. In vitro transfection experiment showed that the G-to-A variation causes a 58% reduction in the promoter activity. After oral glucose challenge, the homozygous A/A subjects had the highest stimulated insulin levels at 60 and 90 minutes and the highest insulin area under the curve as compared to the subjects with other genotypes, which suggested the homozygous A/A subjects were more insulin resistant. As insulin resistance is a risk factor of NIDDM, we concluded that this promoter variation is a risk factor for NIDDM.
    Biochemical and Biophysical Research Communications 05/1996; 221(3):614-8. · 2.28 Impact Factor

Publication Stats

44 Citations
5.38 Total Impact Points

Institutions

  • 1996–1997
    • University of California, Los Angeles
      • Department of Medicine
      Los Angeles, CA, United States