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
1939-327X
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
Socio Economic Objective 970106 Expanding Knowledge in the Biological Sciences
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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