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Am J Physiol Endocrinol Metab 288: E798-E804, 2005. First published December 7, 2004; doi:10.1152/ajpendo.00446.2004
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Isoproterenol decreases leptin release from rat and human adipose tissue through posttranscriptional mechanisms

Matthew R. Ricci,1,* Mi-Jeong Lee,1,* Colleen D. Russell,1 Yanxin Wang,1 Sean Sullivan,1 Stephen H. Schneider,2 Robert E. Brolin,3 and Susan K. Fried1,4

1Department of Nutritional Sciences, Rutgers University 2Division of Endocrinology 3Department of Surgery, University of Medicine and Dentistry of New Jersey, New Brunswick, New Jersey 4Division of Gerontology, Department of Medicine, University of Maryland School of Medicine and Baltimore Veterans Affairs Medical Center, Baltimore, Maryland

Submitted 22 September 2004 ; accepted in final form 30 November 2004

In vivo and in vitro studies indicate that {beta}-adrenergic receptor agonists decrease leptin release from fat cells in as little as 30 min. Our objective was to determine whether alterations in leptin biosynthesis or secretion were involved in the short-term adrenergic regulation of leptin in human and rat adipose tissue. Isoproterenol (Iso) decreased leptin release from incubated adipose tissue of both nonobese and obese subjects to similar extent (–28 vs. –21% after 3 h). Inhibition of protein synthesis with cycloheximide did not block the effect of Iso on leptin release from human adipose tissue, suggesting that the Iso effect is independent of leptin synthesis. Iso also tended to increase tissue leptin content at the end of the 3-h incubation, as expected from the observed inhibition of release. Consistent with a posttranslational mechanism, Iso treatment did not affect leptin mRNA levels or relative rate of leptin biosynthesis as directly assessed by [35S]methionine incorporation into immunoprecipitable leptin. In contrast to these results in human adipose tissues, Iso did not decrease basal leptin release from rat adipose tissue. However, Iso did decrease insulin-stimulated leptin release by inhibiting the ability of insulin to increase leptin biosynthesis without detectably affecting leptin mRNA levels. Thus, in both human and rat, adrenergic regulation of posttranscriptional events (secretion in humans, translation in rats) may contribute to the rapid decline in circulating leptin that occurs when the sympathetic nervous system is activated, such as during fasting and cold exposure. Furthermore, the rat does not provide an ideal model to study mechanisms of cellular leptin regulation in humans.

adipocytes; {beta}-adrenergic receptor


Address for reprint requests and other correspondence: S. K. Fried, Dept. of Medicine, Division of Gerontology, Univ. of Maryland School of Medicine, Baltimore Veterans Affairs Medical Center, GRECC (BT/GR/18), 10 North Greene St., Baltimore, MD 21201 (E-mail: sfried{at}grecc.umaryland.edu)




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