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Modulation of fatty acid induced oxidative stress by adiponectin in 3T3 L1 adipocytes
Author(s) -
Faris Richard Joel,
Davis Jeremy,
Braucher Doug,
WalkerDaniels Jennifer,
Spurlock 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.907.10
Subject(s) - adiponectin , medicine , endocrinology , tlr2 , adipokine , oxidative stress , inflammation , chemistry , adipocyte , adiponectin receptor 1 , cytokine , adipose tissue , tlr4 , biology , insulin resistance , diabetes mellitus
Stimulation of toll‐like receptor signaling by palmitate increases inflammation in adipocytes. Adiponectin is an anti‐inflammatory adipokine. We hypothesized that treatment of adipocytes with palmitate (0.5 mM) would increase production of ROS and transcript levels of iNOS, TLR2 and 4 while decreasing transcript levels of IL10, and that co‐treatment with adiponectin (30 ?g/mL Adn + Palm) would alleviate inflammation and normalize gene expression. We used 10‐day post differentiation mouse 3T3 L1 adipocytes for our studies. Adiponectin decreased ROS production (p=0.0395) while palmitate did not affect ROS production. Treatment with Adn + Palm decreased ROS production compared to palmitate (Palm) alone (p=0.0156). Adiponectin treatment did not affect iNOS, TLR2, or TLR4 transcript levels. Palmitate treatment did not affect TLR2 transcript levels, but there was a trend toward an increase in both iNOS and TLR4 transcript expression (p=0.0616 and 0.0697, respectively). Adiponectin did not alter IL10 expression. Palmitate reduced IL10 transcript abundance as compared with the vehicle control (p=0.0111), and adiponectin reversed this effect. These data suggest that palmitate reduces anti‐inflammatory cytokine production and increases oxidative stress in adipocytes. Adiponectin may have an important role in attenuating the adverse effects of palmitate.