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1 Department of Medicine, University of Maryland at Baltimore, Baltimore, MD, USA; Department of Nutritional Sciences, Rutgers University, New Brunswick, NJ, USA; Department of Endocrinology, University of Medicine and Dentistry of New Jersey, New Brunswick, NJ, USA
* To whom correspondence should be addressed. E-mail: sfried{at}grecc.umaryland.edu.
In vivo and in vitro studies indicate that 
-adrenergic receptor agonists decrease
leptin release from fat cells in as little as 30 minutes. Our objective was to determine if
alterations in leptin biosynthesis or secretion were involved in the short-term adrenergic
regulation of leptin in human and rat adipose tissue. Iso decreased leptin release from
incubated adipose tissue of both non-obese and obese subjects to similar extent (-28% vs.
-21% after 3h). Inhibition of protein synthesis with cycloheximide (CHX) did not block
the effect of Iso on leptin release from human adipose tissue, suggesting Iso effect is
independent of leptin synthesis. Iso also tended to increase tissue leptin content at the end
of the 3h incubation, as expected from the observed inhibition of release. Consistent with
a post-translational 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 post-transcriptional events (secretion in human, 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.
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