, Volume 43, Issue 3, pp 586–592 | Cite as

Racial differences in adiponectin and leptin in healthy premenopausal women

  • Maria AzradEmail author
  • Barbara A. Gower
  • Gary R. Hunter
  • Tim R. Nagy
Original Article


The aim of this article is to longitudinally investigate racial differences in serum adiponectin and leptin in European-American (EA) and African-American (AA) women in the overweight and weight-reduced states. Sixty-two EA and 58 AA premenopausal women were weight reduced from body mass index (BMI) 27–30 kg/m2 to BMI ≤ 24. Fasting serum adiponectin and leptin were determined; body composition and intra-abdominal adipose tissue (IAAT) were measured with dual-energy X-ray absorptiometry and computed tomography, respectively. In repeated-measure MANOVA, there was a significant race effect for IAAT and total fat mass; compared to AA women, EA women had higher IAAT and total fat mass (p < 0.0001 and p = 0.027, respectively). In the mixed-model for adiponectin that adjusted for IAAT, limb fat, and total fat, race was significantly associated with adiponectin (p = 0.046). AA women had significantly lower adjusted adiponectin compared to EA women at baseline [7.67 (6.85, 8.60) vs. 9.32 (8.34, 10.4) μg/ml, p < 0.05] and following weight loss [9.75 (8.70, 10.9) vs. 11.8 (10.6, 13.2) μg/ml, p < 0.05]. In a mixed-model for leptin that adjusted for insulin, estradiol, and fat mass, race was significantly associated with leptin (p < 0.0001). AA women had significantly higher adjusted leptin compared to EA women at baseline [24.7 (22.3, 27.4) vs. 19.9 (18.1, 21.8) ng/dl, p < 0.05] and following weight loss [11.7 (10.2, 13.3) vs. 8.48 (7.50, 9.57) ng/dl, p < 0.05]. Despite having a more favorable body fat distribution, AA women had lower adjusted adiponectin and higher leptin. Differences in body composition and fat distribution do not appear to be significant factors in explaining lower adiponectin and higher leptin in AA women.


Adiponectin Leptin Body composition Ethnicity Obesity 



The authors would like to thank RO1DK49779, NCI Cancer Prevention & Control Training Program [R25 CA047888], UAB Nutrition and Obesity Research Center [P30 DK56336], UAB Diabetes Research and Training Center [P60 DK079626], and UL 1RR025777 for core lab support. The opinions expressed herein are those of the authors and not necessarily those of the NIH or any other organization with which the authors are affiliated. Maria Azrad (MA) conceived the idea to test the hypothesis in the manuscript and constructed the text and tables of the manuscript. Barbara A. Gower and Gary R. Hunter provided MA with access to the database and biological samples used in this manuscript and assisted in editing the manuscript. Tim R. Nagy oversaw the construction of the manuscript and helped in editing the final draft.

Conflict of interest

The authors have no disclosures or conflicts of interest.


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Copyright information

© Springer Science+Business Media, LLC 2012

Authors and Affiliations

  • Maria Azrad
    • 1
    Email author
  • Barbara A. Gower
    • 1
  • Gary R. Hunter
    • 2
  • Tim R. Nagy
    • 1
  1. 1.Department of Nutrition SciencesUniversity of AlabamaBirminghamUSA
  2. 2.Department of Human StudiesUniversity of AlabamaBirminghamUSA

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