<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>Dulloo, Abdul G.</dc:creator>
  <dc:date>2006</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">Catch-up growth during infancy and childhood is increasingly recognized as a major  risk factor for later development of insulin-related complications and chronic diseases,  namely abdominal obesity, type 2 diabetes and cardiovascular disease. As catch-up  growth per se is characterized by insulin resistance, hyperinsulinaemia and an  accelerated rate of fat storage (i.e., catch-up fat) even in the absence of hyperphagia,  the possibility arises that suppressed thermogenesis in certain organs/tissues - for the  purpose of enhancing the efficiency of catch-up fat - also plays a role in the  pathophysiological consequences of catch-up growth. Here, the evidence for the  existence of an adipose-specific control of thermogenesis, the suppression of which  contributes to catch-up fat, is reviewed. Recent findings suggest that such  suppression of thermogenesis is accompanied by hyperinsulinaemia, insulin  resistance in skeletal muscle and insulin hyperresponsiveness in adipose tissue, all of  which precede the appearance of excess body fat, central fat distribution and  elevations in intramyocellular triglyceride or circulating lipid concentrations. These  findings underscore a role for suppressed thermogenesis per se as an early event in  the pathophysiology of catch-up growth. It is proposed that, in its evolutionary  adaptive role to spare glucose for the rapid rebuilding of an adequate fat reserve (for  optimal survival capacity during intermittent famine), suppressed thermogenesis in  skeletal muscle constitutes a thrifty phenotype that confers to the phase of catch-up  growth its high sensitivity to the development of insulin resistance and  hyperinsulinaemia. In the context of the complex interactions between earlier  reprogramming and a modern lifestyle characterized by nutritional abundance and low  physical activity, this thrifty 'catch-up fat phenotype' is a central event that predisposes  individuals with catch-up growth to abdominal obesity, type 2 diabetes and  cardiovascular disease.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://folia.unifr.ch/global/documents/300022</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/300022/files/dulloo_rfs.pdf</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1159/000091512</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>License undefined</dc:rights>
  <dc:source>Hormone Research. - 2006, vol. 65, no. 3, p. 90-97</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">Catch-up growth</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">Low birth weight</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">Obesity</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">Thermogenesis</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">Type 2 diabetes</dc:subject>
  <dc:subject>info:eu-repo/classification/udc/61</dc:subject>
  <dc:title xmlns:ns6="xml" ns6:lang="en">Regulation of fat storage via suppressed thermogenesis: a thrifty phenotype that predisposes individuals with catch-up growth to insulin resistance and obesity</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
