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Redistribution of glucose from skeletal muscle to adipose tissue during catch-up fat. A link between catch-up growth and later metabolic syndrome.

Cettour-Rose, Philippe, Sonia, Sonia, Russell, Aaron, Summermatter, Serge, Mainieri, Davide, Carrillo-Theander, Claudia, Montani, Jean-Pierre, Seydoux, Josiane, Rohner-Jeanrenaud, Françoise and Dulloo, Abdul G. 2005, Redistribution of glucose from skeletal muscle to adipose tissue during catch-up fat. A link between catch-up growth and later metabolic syndrome., Diabetes, vol. 54, pp. 751-756.

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Title Redistribution of glucose from skeletal muscle to adipose tissue during catch-up fat. A link between catch-up growth and later metabolic syndrome.
Author(s) Cettour-Rose, Philippe
Sonia, Sonia
Russell, Aaron
Summermatter, Serge
Mainieri, Davide
Carrillo-Theander, Claudia
Montani, Jean-Pierre
Seydoux, Josiane
Rohner-Jeanrenaud, Françoise
Dulloo, Abdul G.
Journal name Diabetes
Volume number 54
Start page 751
End page 756
Publisher American Diabetes Association
Place of publication New York, N.Y.
Publication date 2005-03
ISSN 0012-1797
Summary 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.
Language eng
Field of Research 060199 Biochemistry and Cell Biology not elsewhere classified
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2005, American Diabetes Association, Inc.
Persistent URL http://hdl.handle.net/10536/DRO/DU:30009119

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Created: Mon, 13 Oct 2008, 15:51:40 EST