Study of the proinflammatory role of human differentiated omental adipocytes

J Cell Biochem. 2009 Aug 15;107(6):1107-17. doi: 10.1002/jcb.22208.


Infiltration of monocyte-derived macrophages into adipose tissue has been associated with tissue and systemic inflammation. It has been suggested that macrophage infiltration affects fat expansion through a paracrine action on adipocyte differentiation. Our working hypothesis is that factors released by monocytes/macrophages may also affect mature adipocyte biology. Human differentiated omental adipocytes were incubated with LPS and conditioned media obtained from human macrophage-like cell line THP-1, previously activated or not with LPS. We show that LPS greatly increased the secretion levels of pro-inflammatory adipokines including IL-6, IL-8, GRO, and MCP-1. Macrophage-conditioned medium also upregulated IL-6, IL-8, GRO, and MCP-1 mRNA expression and protein levels and led to the novo secretion of ICAM-1, IL-1 beta, IP-10, MIP-1 alpha, MIP-1 beta, VEGF, and TNFalpha. Human differentiated adipocytes treated by macrophage-conditioned medium displayed marked reduction of adipocyte function as assessed by decreased phosphorylation levels of ERK1, ERK2, and p38 alpha and reduced gene expression of lipogenic markers including PPAR-gamma and fatty acid synthase. These data show that macrophage-secreted factors not only inhibit the formation of mature adipocytes but alter their function, suggesting that human differentiated omental adipocytes might also contribute to systemic chronic low-grade inflammation associated with human obesity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / pathology*
  • Adipokines / genetics
  • Cell Differentiation
  • Cells, Cultured
  • Cytokines / genetics
  • Gene Expression Profiling
  • Gene Expression Regulation / drug effects
  • Humans
  • Inflammation / etiology*
  • Lipopolysaccharides / pharmacology
  • Macrophages / metabolism
  • Obesity / pathology
  • Omentum / pathology*
  • RNA, Messenger / analysis


  • Adipokines
  • Cytokines
  • Lipopolysaccharides
  • RNA, Messenger