Abstract

Abstract Background: Adipokines, specifically leptin and adiponectin, are directly linked to obesity and it has been suggested that they may contribute to breast carcinogenesis as well. High plasma leptin and low adiponectin concentrations are associated with high levels of body fat, and similar associations have been reported for breast cancer risk. However, little is known about the concentrations of these hormones in breast tissue and if they influence the tissue microenvironment to modify breast cancer risk. Moreover, few studies have investigated racial/ethnic differences in adipokine concentrations and how these differences determine adipokine predictors in different groups. Methods: Plasma and breast tissues collected from one hundred twelve women (67 European American (EA) women and 45 African American (AA) women), without breast cancer, undergoing reduction mammoplasty surgery were analyzed for leptin and adiponectin concentrations. Tissue and plasma leptin and adiponectin were quantified by commercially available enzyme-linked immunosorbent assays (R&D Systems, Minneapolis, MN). Tissue adipokine concentrations were adjusted by total protein concentration (reported as nanograms of hormone per milligram of protein (ng/mg of protein)). Assays were highly reproducible and all CVs were ≤9.3%. Spearman rank correlation coefficients were used to describe associations between plasma and tissue adipokine concentrations as well as associations among adipokine concentrations and selected breast cancer risk variables. Two-way ANOVAs were used to determine associations between adipokine concentrations and race and obesity status. Results: Overall, AAs had significantly higher plasma and tissue leptin and lower plasma adiponectin concentrations than EAs. They also had significantly lower adiponectin to leptin ratios in both plasma and tissue. There was no significant difference in tissue adiponectin concentrations between EAs and AAs. Obese women had significantly higher plasma and tissue leptin than non-obese women, but no significant difference in plasma and tissue adiponectin concentrations were observed. Generally, there were several significant associations observed among plasma and tissue adipokines and selected breast cancer risk variables; however several of these associations were attenuated in AAs and non-obese women. Plasma and tissue leptin correlated well in EAs, but not in AAs. There was no correlation between plasma and tissue adiponectin concentrations in any individual group, but when combined there was a marginal association. Conclusions: We found differences by race/ethnicity and by obesity status in adipokines in tissue and blood. Additionally, we found a lack of association between circulating adiponectin and breast tissue levels for AA women. If adipokines play a role in carcinogenesis in the breast, there may be effect modification by race/ethnicity and by body weight. Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):A88.

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