title: Bisphenol A at environmentally relevant doses inhibits adiponectin release from human adipose tissue explants and adipocytes.
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.
  
  
  OBJECTIVE
  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.
authors.affiliation: Department of Cell and Cancer Biology, University of Cincinnati, 3125 Eden Avenue, Cincinnati, OH 45267, USA.
authors.forename: Eric R
authors.initials: ER
authors.lastname: Hugo
authors.forename: Terry D
authors.initials: TD
authors.lastname: Brandebourg
authors.forename: Jessica G
authors.initials: JG
authors.lastname: Woo
authors.forename: Jean
authors.initials: J
authors.lastname: Loftus
authors.forename: J Wesley
authors.initials: JW
authors.lastname: Alexander
authors.forename: Nira
authors.initials: N
authors.lastname: Ben-Jonathan
mesh_terms: D052242:Adiponectin / Q000037:antagonists & inhibitors* / Q000378:metabolism; D000273:Adipose Tissue / Q000187:drug effects* / Q000378:metabolism; D001483:Base Sequence; D001559:Benzhydryl Compounds; D017931:DNA Primers; D052244:Endocrine Disruptors / Q000633:toxicity*; D004958:Estradiol / Q000494:pharmacology; D006801:Humans; D010636:Phenols / Q000633:toxicity*; D016133:Polymerase Chain Reaction; D000098826:Bisphenol A Compounds
chemical_list: D052242:Adiponectin; D001559:Benzhydryl Compounds; D017931:DNA Primers; D052244:Endocrine Disruptors; D004958:Estradiol; D010636:Phenols; C006780:bisphenol A; D000098826:Bisphenol A Compounds