4.7 Article

Race Differences in the Association of Oxidative Stress With Insulin Sensitivity in African- and European-American Women

Journal

OBESITY
Volume 20, Issue 5, Pages 972-977

Publisher

WILEY
DOI: 10.1038/oby.2011.355

Keywords

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Funding

  1. [2T32DK062710-07]
  2. [R01DK58278]
  3. [M01-RR-00032]
  4. [UL 1RR025777]
  5. [P30-DK56336]
  6. [P60DK079626]

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Excessive metabolism of glucose and/or fatty acids may impair insulin signaling by increasing oxidative stress. The objective of this study was to examine the association between insulin sensitivity and protein carbonyls, a systemic marker of oxidative stress, in healthy, nondiabetic women, and to determine if the relationship differed with race. Subjects were 25 African-Americans (AA, BMI 28.4 +/- 6.2 kg/m(2), range 18.8-42.6 kg/m(2); age 33.1 +/- 13.5 years, range 18-58 years) and 28 European-Americans (EA, BMI 26.2 +/- 5.9 kg/m(2), range 18.7-48.4 kg/m(2); age 31.6 +/- 12.4 years, range 19-58 years). Insulin sensitivity was determined using an intravenous glucose tolerance test incorporating [6,6-H-2(2)]-glucose, and a two-compartment mathematical model. Multiple linear regression results indicated that insulin sensitivity was inversely associated with protein carbonyls in AA (standardized regression coefficient -0.47, P < 0.05) but not EA (0.01, P = 0.945), after adjusting for %body fat. In contrast, %body fat was significantly and positively associated with insulin sensitivity in EA (-0.54, P < 0.01) but not AA (-0.24, P = 0.196). Protein carbonyls were associated with free fatty acids (FFA) in AA (r = 0.58, P < 0.01) but not EA (r = -0.11, P = 0.59). When subjects were divided based on median levels of fasting glucose and FFA, those with higher glucose/FFA concentrations had a significantly greater concentration of circulating protein carbonyls compared to those with lower glucose/FFA concentrations (P < 0.05). These results suggest that oxidative stress independently contributes to insulin sensitivity among AA women. Further, this association in AA may be mediated by circulating FFA and/or glucose.

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