Effect of PEA on LPS inflammatory action in human adipocytes.
N-Palmitoylethanolamide (PEA) is an endogenous lipid secreted by human adipocytes that possesses numerous anti-inflammatory properties. Human adipose tissue can be subjected to modulation of its inflammatory state by lipopolysaccharide (LPS). Here we demonstrate that LPS increases the secretion of interleukin-6 (IL-6) by human mature adipocytes via activation of the NFkappaB pathway. This effect is not inhibited by PEA. Inversely, LPS strongly inhibits adipose cell leptin release, with PEA acting as a potentiator of this inhibitory effect. These actions are not linked to a reduction in leptin gene transcription. Thus, PEA does not have an anti-inflammatory role in the secretion of IL-6 via NFkappaB at the adipocyte level, but instead seems to act at the heart of the LPS-stimulated pathway, which, independently of NFkappaB, inhibits the secretion of leptin.
Hoareau
Laurence
L
Laboratoire de Biochimie et de Génétique Moléculaire, EA-2526, Faculté des Sciences, Université de La Réunion, Saint Denis, France.
Ravanan
Palaniyandi
P
Gonthier
Marie Paule
MP
Delarue
Pierre
P
Gonçalves
José
J
Césari
Maya
M
Festy
Franck
F
Roche
Régis
R
D017667:Adipocytes / Q000187:drug effects* / Q000378:metabolism; D000328:Adult; D000577:Amides; D002478:Cells, Cultured; D063388:Endocannabinoids; D004983:Ethanolamines; D006801:Humans; D007249:Inflammation / Q000139:chemically induced; D015850:Interleukin-6 / Q000378:metabolism; D020738:Leptin / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008875:Middle Aged; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism; D010169:Palmitic Acids / Q000494:pharmacology*
D000577:Amides; D063388:Endocannabinoids; D004983:Ethanolamines; D015850:Interleukin-6; D020738:Leptin; D008070:Lipopolysaccharides; D016328:NF-kappa B; D010169:Palmitic Acids; C005958:palmidrol