PMID- 9564834
OWN - NLM
STAT- MEDLINE
DCOM- 19980508
LR  - 20181201
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 139
IP  - 5
DP  - 1998 May
TI  - In vivo and in vitro evidence for the involvement of tumor necrosis factor-alpha 
      in the induction of leptin by lipopolysaccharide.
PG  - 2278-83
AB  - 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, i.p. 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.
FAU - Finck, B N
AU  - Finck BN
AD  - Department of Animal Sciences, University of Illinois, Urbana 61801, USA.
FAU - Kelley, K W
AU  - Kelley KW
FAU - Dantzer, R
AU  - Dantzer R
FAU - Johnson, R W
AU  - Johnson RW
LA  - eng
GR  - DK-49311/DK/NIDDK NIH HHS/United States
GR  - DK-51576/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Insulin)
RN  - 0 (Leptin)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Proteins)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - PDC6A3C0OX (Glycerol)
SB  - IM
MH  - Adipocytes/metabolism
MH  - Animals
MH  - Cells, Cultured
MH  - Escherichia coli
MH  - Flow Cytometry
MH  - Glycerol/metabolism
MH  - Insulin/pharmacology
MH  - Kinetics
MH  - Leptin
MH  - Lipolysis
MH  - Lipopolysaccharides/*pharmacology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C3H
MH  - *Protein Biosynthesis
MH  - Proteins/metabolism
MH  - Recombinant Proteins/pharmacology
MH  - Tumor Necrosis Factor-alpha/biosynthesis/*pharmacology
EDAT- 1998/05/16 00:00
MHDA- 1998/05/16 00:01
CRDT- 1998/05/16 00:00
PHST- 1998/05/16 00:00 [pubmed]
PHST- 1998/05/16 00:01 [medline]
PHST- 1998/05/16 00:00 [entrez]
AID - 10.1210/endo.139.5.6012 [doi]
PST - ppublish
SO  - Endocrinology. 1998 May;139(5):2278-83. doi: 10.1210/endo.139.5.6012.