<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Casals-Casas C</dc:creator>
  <dc:creator>Desvergne B</dc:creator>
  <dc:date>2011</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">Synthetic chemicals currently used in a variety of industrial and agricultural applications are leading to widespread contamination of the environment. Even though the intended uses of pesticides, plasticizers, antimicrobials, and flame retardants are beneficial, effects on human health are a global concern. These so-called endocrine-disrupting chemicals (EDCs) can disrupt hormonal balance and result in developmental and reproductive abnormalities. New in vitro, in vivo, and epidemiological studies link human EDC exposure with obesity, metabolic syndrome, and type 2 diabetes. Here we review the main chemical compounds that may contribute to metabolic disruption. We then present their demonstrated or suggested mechanisms of action with respect to nuclear receptor signaling. Finally, we discuss the difficulties of fairly assessing the risks linked to EDC exposure, including developmental exposure, problems of high- and low-dose exposure, and the complexity of current chemical environments.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://sonar.ch/global/documents/293588</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1146/annurev-physiol-012110-142200</dc:relation>
  <dc:relation>info:eu-repo/semantics/altIdentifier/pmid/21054169</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:source>Annual review of physiology. - 2011</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">Animals</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">Diabetes Mellitus, Type 2</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">Endocrine Disruptors</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">Environmental Exposure</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">Environmental Pollutants</dc:subject>
  <dc:subject xmlns:ns6="xml" ns6:lang="en">Female</dc:subject>
  <dc:subject xmlns:ns7="xml" ns7:lang="en">Humans</dc:subject>
  <dc:subject xmlns:ns8="xml" ns8:lang="en">Male</dc:subject>
  <dc:subject xmlns:ns9="xml" ns9:lang="en">Metabolic Syndrome</dc:subject>
  <dc:subject xmlns:ns10="xml" ns10:lang="en">Mice</dc:subject>
  <dc:subject xmlns:ns11="xml" ns11:lang="en">Obesity</dc:subject>
  <dc:subject xmlns:ns12="xml" ns12:lang="en">Rats</dc:subject>
  <dc:subject xmlns:ns13="xml" ns13:lang="en">Receptors, Cytoplasmic and Nuclear</dc:subject>
  <dc:subject xmlns:ns14="xml" ns14:lang="en">Signal Transduction</dc:subject>
  <dc:title xmlns:ns15="xml" ns15:lang="en">Endocrine disruptors: from endocrine to metabolic disruption.</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>