Serum Asymmetric Dimethylarginine and Nitric Oxide Levels in Obese Postmenopausal Women

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Kocak H., Oner-Iyidogan Y. , Gurdol F., Oner P., Esin D.

JOURNAL OF CLINICAL LABORATORY ANALYSIS, vol.25, no.3, pp.174-178, 2011 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 25 Issue: 3
  • Publication Date: 2011
  • Doi Number: 10.1002/jcla.20452
  • Page Numbers: pp.174-178


Background: It has been reported that estrogen deficiency after menopause might cause a decrement in nitric oxide (NO) bioavailability by increasing the level of asymmetric dimethylarginine (ADMA), a major endogenous nitric oxide synthase inhibitor, thus leading to abnormalities in endothelial function. Because NO plays an important role on feeding behavior, ADMA may be involved in the pathogenesis of obesity, too. This cross-sectional study aimed to evaluate the relations of ADMA and NO with the obesity-linked peptides, such as ghrelin, leptin, and adiponectin in postmenopausal women free of hormone replacement therapy. Methods: Adiponectin, ghrelin, leptin, ADMA, and NO(x) (total nitrite/nitrate) were measured in 22 obese (BMI: 30-47 kg/m(2)) and 19 normal weight (BMI: 21.5-26 kg/m(2)) postmenopausal women. Anthropometric measurements (height, weight, BMI, waist, and hip circumferences) were recorded. Statistics were made by the Mann-Whitney U-test. Results: Ghrelin and adiponectin levels were significantly lower (P<0.001), whereas ADMA and leptin levels were higher in obese women than in normal weight controls (P<0.01 and 0.001, respectively). BMI was correlated negatively with adiponectin and ghrelin and positively with ADMA and leptin levels. No correlation existed between ADMA and NO. Conclusion: Estrogen deficiency alone may not cause an increase in ADMA levels unless the women are prone to disturbances in energy homeostasis. In spite of the high ADMA levels, the unaltered NO levels in plasma may be owing to ongoing inflammatory conditions. J. Clin. Lab. Anal. 25:174-178, 2011. (C) 2011 Wiley-Liss, Inc.