The effects of bisphenol A (BPA) exposure on fat mass and serum leptin concentrations have no impact on bone mineral densities in non-obese premenopausal women
ABSTRACT OBJECTIVES: Bisphenol A (BPA) exposure may promote obesity, but its effect on bone mineral density (BMD) has not been reported in humans. We aimed to examine the relationships between BPA exposure, body composition, serum estradiol, leptin, osteocalcin levels and BMDs in healthy premenopausal women. DESIGN AND METHODS: In this cross-sectional study, a total of 246 healthy premenopausal women aged 20years and older with regular menstrual cycles were investigated. Body mass index (BMI), fat mass, fat-free mass and BMDs were measured by DXA. Serum estradiol, leptin, osteocalcin, urinary BPA and NTx levels were also tested. RESULTS: Urinary BPA levels were positively associated with fat mass (r=0.193, p=0.006) and leptin (r=0.236, p=0.001) but not with fat-free mass after adjusting for age and BMI. BPA was not associated with serum estradiol levels, BMDs, or bone resorption marker NTx and bone formation parameter osteocalcin, either. A multivariate stepwise regression analysis confirmed that serum leptin levels were positively influenced by fat mass (β=0.746, p<0.001) and BPA (β=0.127, p=0.01) but negatively correlated with fat-free mass (β=-0.196, p<0.001). However, the changes of BMDs at the lumbar spine (β=0.298, p<0.001) and femoral neck (β=0.305, p<0.001) were primarily explained by fat-free mass, and were irrelevant of the fat mass, leptin or BPA exposure. CONCLUSIONS: Although BPA exposure is related with increased amount of fat mass and elevated serum leptin levels, it has neutral effect on BMDs in premenopausal women, possibly due to the exclusive role of fat-free mass, which is unrelated to BPA in determining BMDs.
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ABSTRACT: Abstract Introduction: Bisphenol A (BPA), a high-volume chemical with weak estrogenic properties, has been linked to obesity, cardiovascular diseases (CVD) and diabetes mellitus (DM). This review evaluates both the consistency and the quality of epidemiological evidence from studies testing the hypothesis that BPA exposure is a risk factor for these health outcomes. Methods: We followed the current methodological guidelines for systematic reviews by using two independent researchers to identify, review and summarize the relevant epidemiological literature on the relation of BPA to obesity, CVD, DM, or related biomarkers. Each paper was summarized with respect to its methods and results with particular attention to study design and exposure assessment, which have been cited as the main areas of weakness in BPA epidemiologic research. As quantitative meta-analysis was not feasible, the study results were categorized qualitatively as positive, inverse, null, or mixed. Results: Nearly all studies on BPA and obesity-, DM- or CVD-related health outcomes used a cross-sectional design and relied on a single measure of BPA exposure, which may result in serious exposure misclassification. For all outcomes, results across studies were inconsistent. Although several studies used the same data and the same or similar statistical methods, when the methods varied slightly, even studies that used the same data produced different results. Conclusion: Epidemiological study design issues severely limit our understanding of health effects associated with BPA exposure. Considering the methodological limitations of the existing body of epidemiology literature, assertions about a causal link between BPA and obesity, DM, or CVD are unsubstantiated.Critical Reviews in Toxicology 01/2014; 44(2). DOI:10.3109/10408444.2013.860075 · 6.41 Impact Factor
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ABSTRACT: BACKGROUND:: Bisphenol A (BPA) is an endocrine disruptor that in animal studies can bind to the thyroid hormone receptor and affect thyroid function. Relevant epidemiologic studies are limited and results are inconsistent. We explored the relationship between urinary BPA and thyroid function in a Chinese population. METHODS:: The study population included 3394 subjects age 40 years or older who were enrolled in a population-based study from Songnan Community, Baoshan District, Shanghai, China, from June through August 2009. We analyzed the association between urinary BPA and thyroid function using multivariate linear regression. Participants were further divided according to thyroid function status, and logistic regression was applied to determine the relationship between urinary BPA and thyroid function. RESULTS:: Each one-quartile increase in BPA was related to an increase of 0.068 pmol/l (95% confidence interval = 0.065- 0.071) in free triiodothyronine and a 0.084 μIU/ml decline (-0.099 to -0.069) in thyroid-stimulating hormone (TSH) in men. For women, there was a 0.10 pmol/l (0.09 to 0.11) increase in free triiodothyronine and a 0.13 μIU/ml decline (-0.14 to -0.11) in TSH. High urinary BPA level was associated with increased thyroid function (adjusted odds ratio = 1.71 [1.26 to 2.32]). CONCLUSIONS:: Our results support previous reports of associations between BPA exposure and altered thyroid hormones in animal models and epidemiologic studies. Because our study is cross-sectional, no causal relationships can be established.Epidemiology (Cambridge, Mass.) 01/2013; 24(2). DOI:10.1097/EDE.0b013e318280e02f · 6.18 Impact Factor
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ABSTRACT: Bisphenol A (BPA), a major component of epoxy resins used in protective coatings is known endocrine-disrupting chemical. BPA has the ability of binding to estrogen receptors. In the current paper, we examine the direct effects of bisphenol A on in vitro osteoclast and osteoblast culture systems. We evaluated the effects of BPA on osteoclast formation using bone marrow-derived macrophages and RAW 264.7 cells and on osteoblast differentiation using MC3T3-E1 cells. BPA significantly inhibited RANKL-induced, TRAP-positive multinucleated cell formation in bone marrow-derived macrophages and RAW 264.7 cell cultures in a dose-dependent manner (0.5 uM to 12.5 uM). We observed suppression of ERK, JNK, AKT, and p38 mitogen-activated protein kinases induced by RANKL in Western blotting after BPA treatment in RAW 264.7 cells. Furthermore, BPA suppressed Bcl-2 (anti-apoptotic) while stimulating Bax (pro-apoptotic) protein expression in RAW 264.7 cells. Bisphenol A also significantly suppressed ALP activities and bone nodule formation in MC3T3-E1 cell cultures. Specifically, the expression of Bcl-2 protein was decreased, and changes in expression of caspases 3, 8, and 9 were detected by BPA treatment in both cells. We found that bisphenol A directly suppressed both osteoclastic and osteoblastic activities in vitro. Our data suggest that bisphenol A suppresses cell differentiation and survival.Life sciences 07/2013; 93(9-11). DOI:10.1016/j.lfs.2013.07.020 · 2.30 Impact Factor