title: Exposure to an organometal compound stimulates adipokine and cytokine expression in white adipose tissue.
abstract: OBJECTIVE
  White adipose tissue (WAT) is now considered a defined tissue capable of interactions with other organ systems. WAT role in elevating the level of systemic chronic inflammation suggests that alterations in this tissue as the result of disease or environmental factors may influence the development and progression of various obesity-related pathologies. This study investigated WAT cell-specific responses to an organometal compound, trimethyltin (TMT), to determine possible contribution to induced inflammation.
  
  
  METHODS
  Human primary mature adipocytes and macrophage differentiated THP-1 cells were cultured in TMT presence and relative toxicities and different adipokine levels were determined. The inflammatory response was examined in TMT presence for primary cells from obese ob/ob mice WAT, and after TMT injection in ob/ob mice.
  
  
  RESULTS
  Both adipocytes and macrophages were resistant to cell death induced by TMT. However, adipocytes cultured in TMT presence showed increased expression of TNFα and IL-6, and modified leptin levels. In macrophage cultures, TMT also increased TNFα and IL-6, while MCP-1 and MIP-1α were decreased. In vivo, a single injection of TMT in ob/ob mice, elevated TNFα, MIP-1α and adiponectin in WAT.
  
  
  CONCLUSIONS
  Elevation of the inflammatory related products can be induced by chemical exposure in adipocytes and macrophages, as well as murine WAT. These data suggest that numerous factors, including a systemic chemical exposure, can induce an inflammatory response from the WAT. Furthermore, when characterizing both chemical-induced toxicity and the progression of the chronic inflammation associated with elevated WAT content, such responses in this target tissue should be taken into consideration.
authors.affiliation: Laboratoire de Biochimie et de Génétique Moléculaire, Groupe d'Etude de l'Inflammation Chronique et de l'Obésité, Université de La Réunion, Faculté des Sciences, 15 avenue R. Cassin and Plateforme CYROI, 2 rue Maxime Rivière, 97490 Sainte Clotilde, France.
authors.forename: Palaniyandi
authors.initials: P
authors.lastname: Ravanan
authors.forename: G Jean
authors.initials: GJ
authors.lastname: Harry
authors.forename: Rana
authors.initials: R
authors.lastname: Awada
authors.forename: Laurence
authors.initials: L
authors.lastname: Hoareau
authors.forename: Frank
authors.initials: F
authors.lastname: Tallet
authors.forename: Régis
authors.initials: R
authors.lastname: Roche
authors.forename: Christian
authors.initials: C
authors.lastname: Lefebvre d'Hellencourt
mesh_terms: D017667:Adipocytes / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D054392:Adipokines / Q000235:genetics*; D052242:Adiponectin / Q000235:genetics; D052436:Adipose Tissue, White / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D002460:Cell Line; D045744:Cell Line, Tumor; D002478:Cells, Cultured; D016207:Cytokines / Q000235:genetics*; D005260:Female; D015870:Gene Expression / Q000187:drug effects*; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D015850:Interleukin-6 / Q000235:genetics; D019169:Jurkat Cells; D020738:Leptin / Q000235:genetics; D008264:Macrophages / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008820:Mice, Obese; D009479:Neuropeptides / Q000235:genetics; D052247:Nitric Oxide Synthase Type II / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014298:Trimethyltin Compounds / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D054392:Adipokines; D052242:Adiponectin; D016207:Cytokines; D015850:Interleukin-6; D020738:Leptin; D009479:Neuropeptides; D014298:Trimethyltin Compounds; D014409:Tumor Necrosis Factor-alpha; C046488:trimethyltin; C075692:stannin; D052247:Nitric Oxide Synthase Type II