<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>Marcelino, Helena</dc:creator>
  <dc:creator>Veyrat-Durebex, Christelle</dc:creator>
  <dc:creator>Summermatter, Serge</dc:creator>
  <dc:creator>Sarafian, Delphine</dc:creator>
  <dc:creator>Miles-Chan, Jennifer L.</dc:creator>
  <dc:creator>Arsenijevic, Denis</dc:creator>
  <dc:creator>Zani, Fabio</dc:creator>
  <dc:creator>Montani, Jean-Pierre</dc:creator>
  <dc:creator>Seydoux, Josiane</dc:creator>
  <dc:creator>Solinas, Giovanni</dc:creator>
  <dc:creator>Rohner-Jeanrenaud, Françoise</dc:creator>
  <dc:creator>Dulloo, Abdul G.</dc:creator>
  <dc:date>2012-09-06</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">Catch-up growth, a risk factor for type 2 diabetes, is characterized by  hyperinsulinemia and accelerated body fat recovery. Using a rat model of  semistarvation-refeeding that exhibits catch-up fat, we previously reported that during  refeeding on a low-fat diet, glucose tolerance is normal but insulin-dependent glucose  utilization is decreased in skeletal muscle and increased in adipose tissue, where de  novo lipogenic capacity is concomitantly enhanced. Here we report that isocaloric  refeeding on a high-fat (HF) diet blunts the enhanced in vivo insulin-dependent  glucose utilization for de novo lipogenesis (DNL) in adipose tissue. These are shown  to be early events of catch-up growth that are independent of hyperphagia and  precede the development of overt adipocyte hypertrophy, adipose tissue inflammation,  or defective insulin signaling. These results suggest a role for enhanced DNL as a  glucose sink in regulating glycemia during catch-up growth, which is blunted by  exposure to an HF diet, thereby contributing, together with skeletal muscle insulin  resistance, to the development of glucose intolerance. Our findings are presented as  an extension of the Randle cycle hypothesis, whereby the suppression of DNL  constitutes a mechanism by which dietary lipids antagonize glucose utilization for  storage as triglycerides in adipose tissue, thereby impairing glucose homeostasis  during catch-up growth.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://folia.unifr.ch/global/documents/302965</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/302965/files/dull_rat.pdf</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/302965/files/dull_rat_sm.pdf</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.2337/db12-0255</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>License undefined</dc:rights>
  <dc:source>Diabetes. - 2013, vol. 62, no. 2, p. 362-372</dc:source>
  <dc:subject>info:eu-repo/classification/udc/57</dc:subject>
  <dc:title xmlns:ns1="xml" ns1:lang="en">A role for adipose tissue de novo lipogenesis in glucose homeostasis during catch-up growth : a randle cycle favoring fat storage</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
