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Endocrinology Vol. 139, No. 5 2278-2283
Copyright © 1998 by The Endocrine Society

ARTICLES

In Vivo and in Vitro Evidence for the Involvement of Tumor Necrosis Factor-{alpha} in the Induction of Leptin by Lipopolysaccharide1

Brian N. Finck, Keith W. Kelley, Robert Dantzer and Rodney W. Johnson

Laboratories of Integrative Biology (B.N.F., R.W.J.) and Immunophysiology (K.W.K.) Department of Animal Sciences, University of Illinois, Urbana, Illinois 61801; and the Laboratory of Integrative Neurobiology, INRA-INSERM, U-934 (R.D.), 33077 Bordeaux, France

Address all correspondence and requests for reprints to: Dr. R. W. Johnson, 390 Animal Sciences Laboratory, University of Illinois, 1207 West Gregory Drive, Urbana, Illinois 61801. E-mail: rwjohn{at}uiuc.edu

To examine the role of tumor necrosis factor-{alpha} (TNF{alpha}) in mediating leptin secretion during an immunological challenge, we studied the effects of lipopolysaccharide (LPS) and TNF{alpha} on leptin secretion in endotoxin-sensitive C3H/HeOuJ (OuJ) mice, endotoxin-insensitive C3H/HeJ (HeJ) mice, and primary adipocytes cultured from both. Intraperitoneal injection of LPS increased plasma concentrations of TNF{alpha} and leptin in OuJ mice, but not in HeJ mice, suggesting a causal relationship between the induction of TNF{alpha} and leptin. Consistent with this idea, ip injection of recombinant murine TNF{alpha} increased plasma leptin in both OuJ and HeJ mice. To determine whether TNF{alpha} induces leptin secretion by acting directly on fat cells, primary adipocytes from OuJ and HeJ mice were cultured in the presence of TNF{alpha} or LPS. Whereas LPS was without effect on leptin secretion by adipocytes, TNF{alpha} induced a marked increase in the cell supernatant leptin concentration. These data demonstrate that TNF{alpha} plays a role in regulating the increase in leptin caused by LPS. Moreover, they show that TNF{alpha} can act directly on adipocytes to stimulate leptin secretion. Our results are consistent with the emerging view that leptin is a key hormone coupling immune system activity to energy balance.




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Copyright © 1998 by The Endocrine Society