Redistribution of Glucose From Skeletal Muscle to Adipose Tissue During Catch-Up Fat

A Link Between Catch-Up Growth and Later Metabolic Syndrome

  1. Philippe Cettour-Rose1,
  2. Sonia Samec2,
  3. Aaron P. Russell3,
  4. Serge Summermatter4,
  5. Davide Mainieri4,
  6. Claudia Carrillo-Theander1,
  7. Jean-Pierre Montani4,
  8. Josiane Seydoux2,
  9. Françoise Rohner-Jeanrenaud1 and
  10. Abdul G. Dulloo4
  1. 1Department of Internal Medicine and Department of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, Geneva, Switzerland
  2. 2Department of Physiology, Faculty of Medicine, University of Geneva, Geneva, Switzerland
  3. 3Clinique de réadaptation, SUVA Care, Sion, Switzerland
  4. 4Department of Medicine, Division of Physiology, University of Fribourg, Fribourg, Switzerland
  1. Address correspondence and reprint requests to Dr. Abdul G. Dulloo, Department of Medicine, Division of Physiology, University of Fribourg, Rue du Musée 5, CH-1700 Fribourg, Switzerland. E-mail: abdul.dulloo{at}


Catch-up growth, a risk factor for later obesity, type 2 diabetes, and cardiovascular diseases, is characterized by hyperinsulinemia and an accelerated rate for recovering fat mass, i.e., catch-up fat. To identify potential mechanisms in the link between hyperinsulinemia and catch-up fat during catch-up growth, we studied the in vivo action of insulin on glucose utilization in skeletal muscle and adipose tissue in a previously described rat model of weight recovery exhibiting catch-up fat caused by suppressed thermogenesis per se. To do this, we used euglycemic-hyperinsulinemic clamps associated with the labeled 2-deoxy-glucose technique. After 1 week of isocaloric refeeding, when body fat, circulating free fatty acids, or intramyocellular lipids in refed animals had not yet exceeded those of controls, insulin-stimulated glucose utilization in refed animals was lower in skeletal muscles (by 20–43%) but higher in white adipose tissues (by two- to threefold). Furthermore, fatty acid synthase activity was higher in adipose tissues from refed animals than from fed controls. These results suggest that suppressed thermogenesis for the purpose of sparing glucose for catch-up fat, via the coordinated induction of skeletal muscle insulin resistance and adipose tissue insulin hyperresponsiveness, might be a central event in the link between catch-up growth, hyperinsulinemia and risks for later metabolic syndrome.


    • Accepted December 6, 2004.
    • Received September 30, 2004.
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