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Trans‐10, cis‐12 conjugated linoleic acid (CLA)‐mediated inflammatory signaling: Essential role of human adipocytes in initiating cross‐talk with preadipocytes
Author(s) -
Martinez Kristina Brooke,
Chung Soonkyu,
LaPoint Kathleen,
Kennedy Arion,
WalkerWest Tiffany,
McIntosh Michael
Publication year - 2009
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.23.1_supplement.717.26
Subject(s) - conjugated linoleic acid , lipopolysaccharide , adipose tissue , inflammation , monocyte , endocrinology , chemistry , medicine , cell culture , biology , microbiology and biotechnology , immunology , biochemistry , linoleic acid , fatty acid , genetics
We have previously shown that both lipopolysaccharide (LPS) and CLA, a popular weight loss supplement, activate inflammatory signaling that promote insulin resistance in primary cultures of human (pre)adipocytes. Because our published data demonstrated that preadipocytes were the primary instigators of inflammatory signaling in LPS‐treated cultures, we hypothesized that they played the same role in CLA‐mediated inflammation. To test this hypothesis, we employed two experimental models; Model 1‐ a Co‐Culture Insert Model in which inserts containing ~50% adipocytes (AD50) or ~100% preadipocytes (AD0) were suspended over wells containing AD50 or AD0 cultures, and Model 2‐ a Conditioned Media (CM) Model in which naïve AD0 and AD50 cultures were treated with CM from CLA‐treated AD50 or AD0 cultures. In Model 1, CLA‐induced interleukin (IL)‐8 and IL‐1β mRNA levels were highest in AD50 cultures when co‐cultured with AD0 inserts, whereas no increase in these genes were detected in AD0 cultures. In Model 2, IL‐8 and monocyte chemoattractant protein (MCP)‐1 mRNA levels were increased in cultures treated with CM from CLA‐treated AD50, but not AD0, cultures. These data suggest that, in contrast to LPS, CLA instigates release of inflammatory signals from adipocytes that subsequently activate adjacent preadipocytes in primary cultures of human (pre)adipocytes. Supported by NIH‐NIDDK/ODS 2R01‐DK063070. Grant Funding Source NIH‐NIDDK/ODS 2R01‐ DK063070 and NCARS 06771