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Bisphenol A at environmentally relevant doses inhibits adiponectin release from human adipose tissue explants and adipocytes.

Hugo ER, Brandebourg TD, Woo JG, Loftus J, Alexander JW, Ben-Jonathan N - Environ. Health Perspect. (2008)

Bottom Line: Despite substantial variability among patients, BPA was as effective, and often more effective, than equimolar concentrations of E(2).Adipose tissue expresses similar mRNA levels of ERalpha, ERbeta, and ERRgamma, and 20- to 30-fold lower levels of GPR30, ERRalpha, and ERRbeta.BPA at environmentally relevant doses inhibits the release of a key adipokine that protects humans from metabolic syndrome.

View Article: PubMed Central - PubMed

Affiliation: Department of Cell and Cancer Biology, University of Cincinnati, 3125 Eden Avenue, Cincinnati, OH 45267, USA.

ABSTRACT

Background: The incidence of obesity has risen dramatically over the last few decades. This epidemic may be affected by exposure to xenobiotic chemicals. Bisphenol A (BPA), an endocrine disruptor, is detectable at nanomolar levels in human serum worldwide. Adiponectin is an adipocyte-specific hormone that increases insulin sensitivity and reduces tissue inflammation. Thus, any factor that suppresses adiponectin release could lead to insulin resistance and increased susceptibility to obesity-associated diseases.

Objectives: In this study we aimed to compare a) the effects of low doses of BPA and estradiol (E(2)) on adiponectin secretion from human breast, subcutaneous, and visceral adipose explants and mature adipocytes, and b) expression of putative estrogen and estrogen-related receptors (ERRs) in these tissues.

Methods: We determined adiponectin levels in conditioned media from adipose explants or adipocytes by enzyme-linked immunosorbant assay. We determined expression of estrogen receptors (ERs) alpha and beta, G-protein-coupled receptor 30 (GPR30), and ERRs alpha, beta, and gamma by quantitative real-time polymerase chain reaction.

Results: BPA at 0.1 and 1 nM doses suppressed adiponectin release from all adipose depots examined. Despite substantial variability among patients, BPA was as effective, and often more effective, than equimolar concentrations of E(2). Adipose tissue expresses similar mRNA levels of ERalpha, ERbeta, and ERRgamma, and 20- to 30-fold lower levels of GPR30, ERRalpha, and ERRbeta.

Conclusions: BPA at environmentally relevant doses inhibits the release of a key adipokine that protects humans from metabolic syndrome. The mechanism by which BPA suppresses adiponectin and the receptors involved remains to be determined.

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Related in: MedlinePlus

BPA and E2 suppress adiponectin release from mature abdominal SC adipocytes from a non-obese woman (A) and an obese woman (B). (A) Effect of treatment with increasing doses of BPA or E2. (B) Effect of treatment with increasing doses of BPA, E2, and ICI. Each value is the mean ± SE of four determinations. *p < 0.05 compared with control.
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f3-ehp-116-1642: BPA and E2 suppress adiponectin release from mature abdominal SC adipocytes from a non-obese woman (A) and an obese woman (B). (A) Effect of treatment with increasing doses of BPA or E2. (B) Effect of treatment with increasing doses of BPA, E2, and ICI. Each value is the mean ± SE of four determinations. *p < 0.05 compared with control.

Mentions: In addition to mature adipocytes, adipose tissue contains pre-adipocytes, fibroblasts, endothelial cells, and macrophages, many of which affect the secretory activity of the adipocytes (Fain et al. 2004). Thus, we opted to examine if the above compounds have a direct or an indirect effect on adiponectin release. We isolated mature SC adipocytes from several additional women undergoing abdominoplasty. Figure 3 illustrates the secretory profile of adiponectin from a nonobese patient (Figure 3A; 57 years of age, BMI = 28.8) and an obese patient (Figure 3B; 54 years of age, BMI = 45.2). BPA and E2 significantly inhibited adiponectin release from mature adipocytes at most doses examined, albeit without exhibiting dose-dependent effects. ICI at all doses examined significantly inhibited adiponectin release (Figure 3B).


Bisphenol A at environmentally relevant doses inhibits adiponectin release from human adipose tissue explants and adipocytes.

Hugo ER, Brandebourg TD, Woo JG, Loftus J, Alexander JW, Ben-Jonathan N - Environ. Health Perspect. (2008)

BPA and E2 suppress adiponectin release from mature abdominal SC adipocytes from a non-obese woman (A) and an obese woman (B). (A) Effect of treatment with increasing doses of BPA or E2. (B) Effect of treatment with increasing doses of BPA, E2, and ICI. Each value is the mean ± SE of four determinations. *p < 0.05 compared with control.
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2599757&req=5

f3-ehp-116-1642: BPA and E2 suppress adiponectin release from mature abdominal SC adipocytes from a non-obese woman (A) and an obese woman (B). (A) Effect of treatment with increasing doses of BPA or E2. (B) Effect of treatment with increasing doses of BPA, E2, and ICI. Each value is the mean ± SE of four determinations. *p < 0.05 compared with control.
Mentions: In addition to mature adipocytes, adipose tissue contains pre-adipocytes, fibroblasts, endothelial cells, and macrophages, many of which affect the secretory activity of the adipocytes (Fain et al. 2004). Thus, we opted to examine if the above compounds have a direct or an indirect effect on adiponectin release. We isolated mature SC adipocytes from several additional women undergoing abdominoplasty. Figure 3 illustrates the secretory profile of adiponectin from a nonobese patient (Figure 3A; 57 years of age, BMI = 28.8) and an obese patient (Figure 3B; 54 years of age, BMI = 45.2). BPA and E2 significantly inhibited adiponectin release from mature adipocytes at most doses examined, albeit without exhibiting dose-dependent effects. ICI at all doses examined significantly inhibited adiponectin release (Figure 3B).

Bottom Line: Despite substantial variability among patients, BPA was as effective, and often more effective, than equimolar concentrations of E(2).Adipose tissue expresses similar mRNA levels of ERalpha, ERbeta, and ERRgamma, and 20- to 30-fold lower levels of GPR30, ERRalpha, and ERRbeta.BPA at environmentally relevant doses inhibits the release of a key adipokine that protects humans from metabolic syndrome.

View Article: PubMed Central - PubMed

Affiliation: Department of Cell and Cancer Biology, University of Cincinnati, 3125 Eden Avenue, Cincinnati, OH 45267, USA.

ABSTRACT

Background: The incidence of obesity has risen dramatically over the last few decades. This epidemic may be affected by exposure to xenobiotic chemicals. Bisphenol A (BPA), an endocrine disruptor, is detectable at nanomolar levels in human serum worldwide. Adiponectin is an adipocyte-specific hormone that increases insulin sensitivity and reduces tissue inflammation. Thus, any factor that suppresses adiponectin release could lead to insulin resistance and increased susceptibility to obesity-associated diseases.

Objectives: In this study we aimed to compare a) the effects of low doses of BPA and estradiol (E(2)) on adiponectin secretion from human breast, subcutaneous, and visceral adipose explants and mature adipocytes, and b) expression of putative estrogen and estrogen-related receptors (ERRs) in these tissues.

Methods: We determined adiponectin levels in conditioned media from adipose explants or adipocytes by enzyme-linked immunosorbant assay. We determined expression of estrogen receptors (ERs) alpha and beta, G-protein-coupled receptor 30 (GPR30), and ERRs alpha, beta, and gamma by quantitative real-time polymerase chain reaction.

Results: BPA at 0.1 and 1 nM doses suppressed adiponectin release from all adipose depots examined. Despite substantial variability among patients, BPA was as effective, and often more effective, than equimolar concentrations of E(2). Adipose tissue expresses similar mRNA levels of ERalpha, ERbeta, and ERRgamma, and 20- to 30-fold lower levels of GPR30, ERRalpha, and ERRbeta.

Conclusions: BPA at environmentally relevant doses inhibits the release of a key adipokine that protects humans from metabolic syndrome. The mechanism by which BPA suppresses adiponectin and the receptors involved remains to be determined.

Show MeSH
Related in: MedlinePlus