<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>Dallmann, Robert</dc:creator>
  <dc:creator>Touma, Chadi</dc:creator>
  <dc:creator>Palme, Rupert</dc:creator>
  <dc:creator>Albrecht, Urs</dc:creator>
  <dc:creator>Steinlechner, Stephan</dc:creator>
  <dc:date>2006-02-28</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">Biological clocks have evolved in all kinds of organisms in order to anticipate and adjust to the daily light–dark cycle. Within the last decade, the molecular machinery underlying the circadian system was unraveled. In the present study, the impact of the loss of the &lt;i&gt;Per1&lt;/i&gt; or &lt;i&gt;Per2&lt;/i&gt; genes, key components of the core clock oscillator, on body mass, food and water intake, glucose metabolism, and hypothalamic-pituitary-adrenal axis, was investigated in the &lt;i&gt;Per1&lt;/i&gt; and &lt;i&gt;Per2&lt;/i&gt; mouse models. The results reveal that the lack of &lt;i&gt;Per1&lt;/i&gt; but not &lt;i&gt;Per2&lt;/i&gt; has severe consequences for the regulation of these parameters. Specifically, in &lt;i&gt;Per1&lt;/i&gt; animals, we found an impaired daily glucocorticoid rhythm, with markedly elevated levels during the day compared to control animals. In addition, &lt;i&gt;Per1&lt;/i&gt; mice showed significant differences in body mass as well as food and water intake. Although the &lt;i&gt;Per1&lt;/i&gt; are lighter than wildtype mice, food and water intake per gram body mass is elevated. In addition, the &lt;i&gt;Per1&lt;/i&gt; mice exhibit an increased glucose metabolism after i.p. injection with glucose. In conclusion, our study presents first evidence for a link between an altered metabolism in &lt;i&gt;Per1&lt;/i&gt; and &lt;i&gt;Per2&lt;/i&gt; deficient mice, which in the case of the &lt;i&gt;Per1&lt;/i&gt; animals might be due to an impaired corticosterone rhythm.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://folia.unifr.ch/global/documents/300118</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/300118/files/albrecht_idg.pdf</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1007/s00359-006-0114-9</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>License undefined</dc:rights>
  <dc:source>Journal of Comparative Physiology A: Neuroethology, Sensory, Neural, and Behavioral Physiology. - 2006, vol. 192, no. 7, p. 769-775</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">adrenocortical activity</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">circadian rhythm</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">clock gene</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">fecal glucocorticoid metabolites</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">period</dc:subject>
  <dc:subject>info:eu-repo/classification/udc/57</dc:subject>
  <dc:title xmlns:ns6="xml" ns6:lang="en">Impaired daily glucocorticoid rhythm in &lt;i&gt;Per1&lt;/i&gt;&lt;sup&gt;&lt;i&gt;Brd&lt;/i&gt;&lt;/sup&gt; mice</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
