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Articles in PresS, published online ahead of print December 17, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00368.2002
Submitted on August 19, 2002
Accepted on December 3, 2002
,'-methyl-substituted hexadecanedioic acid (Medica 16) in obese Zucker rats in vivo
1 Department of Human Nutrition and Metabolism, Hebrew University Medical School, Jerusalem, Israel
* To whom correspondence should be addressed. E-mail: bella{at}pob.huji.ac.il.
The putative role played by insulin sensitizers in modulating adipose tissue lipolysis in the fasting state was evaluated here in obese conscious Zucker rats treated with troglitazone or Medica 16 and compared with nontreated lean and obese animals. Ra glycerol, Ra FFA, primary intraadipose reesterification and secondary reuptake of plasma FFA into adipose fat were measured using constant infusion of stable isotope-labeled [2H5]-glycerol, [2,2-2H2]-palmitate and radioactive 3H-palmitate. The overall lipolytic flux (Ra glycerol) was 1.7 and 1.4 fold increased in obese animals treated with troglitazone or Medica 16, respectively, resulting in increased FFA export (RaFFA) in the troglitazone-treated rats. Primary intraadipose reesterification of lipolysis-derived fatty acids was 2 fold enhanced by insulin sensitizers, while reesterification of plasma fatty acids was unaffected by either treatment. In spite of the unchanged Ra FFA in Medica 16 or the increased RaFFA induced by troglitazone, VLDL production rates were robustly curtailed. Total adipose tissue reesterification, used as an estimate of glucose conversion to glycerideglycerol, was 1.9 fold increased by treatment with the insulin sensitizers. Our results indicate that in the fasting state insulin sensitizers induce in vivo a significant activation rather than suppression of adipose tissue lipolysis together with stimulation of glucose conversion to glycerideglycerol.
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