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Interactive Changes between Macrophages and Adipocytes
Author(s) -
Xie Linglin,
Ortega Teresa M.,
Mora Silvia,
Chapes Stephen K.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.686.12
Subject(s) - adipocyte , adipose tissue , adipogenesis , medicine , adipose tissue macrophages , endocrinology , microbiology and biotechnology , macrophage , biology , white adipose tissue , tumor necrosis factor alpha , integrin alpha m , chemistry , glut4 , insulin , in vitro , immunology , flow cytometry , insulin resistance , biochemistry
We tested the hypothesis that communication between macrophages and adipocytes affects insulin response and macrophages function interactively. Firstly, we looked at the impacts of adipocytes on macrophages activation and differentiation. We observed that preadipocytes and adipocytes increased PEC‐C2D macrophage IL‐6 transcript levels, while preadipocytes inhibited IL‐1b transcript levels in co‐culture. We therefore explored the impact of white adipose tissue (WAT) and brown white adipose tissue (BAT) on C2D cells in vivo. After intraperitoneal injection, C2D cells migrated into WAT and BAT. A higher percentage of C2D macrophage cells isolated from WAT expressed Ly‐6C, CD11b, Mac‐2 and F4/80 compared to C2D cultured in vitro, with upregulated transcription levels of inflammatory related genes, but those for BAT isolated C2D is decreased. Secondly, we studied the impact of macrophages on insulin response and differentiation in 3T3L1 adipocytes. Macrophages and recombinant TNF‐a, IL‐1b, and IL‐6 decreased GLUT4 transcript levels in 3T3L1 adipocytes. IL‐6 and TNF‐a, but not IL‐1b, inhibited Akt phosphorylation within 30 min of insulin stimulation. Lastly, adipocyte adipogenesis was inhibited by macrophages or by recombinant TNF‐a, IL‐6, and IL‐1b. These data suggest that macrophages and adipocytes interactively affect insulin signaling, adipocyte differentiation, and macrophage function.