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Oleic acid attenuates trans‐10, cis‐12 (10,12) conjugated linoleic acid (CLA)‐mediated inflammatory signaling in primary human adipocytes
Author(s) -
Reardon Meaghan Ann,
Gobern Semone,
Martinez Kristina,
Chung Chia Chi,
Reid Tanya,
McIntosh Michael
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.995.2
Subject(s) - oleic acid , conjugated linoleic acid , chemistry , linoleic acid , stearic acid , insulin resistance , fatty acid , inflammation , biochemistry , endocrinology , medicine , insulin , biology , organic chemistry
CLA is a popular weight loss supplement consisting of 10,12 and cis‐9, trans‐11 (9,11) isomers that reduces adiposity. However, the consumption of CLA, particularly the 10,12 isomer, is associated with adverse side effects including chronic inflammation and insulin resistance. We hypothesized that these side effects of 10,12 CLA were linked to reduced activity of lipogenic enzymes including stearoyl‐CoA desaturase (SCD)‐1, a delta‐9 desaturase essential for the production of monounsaturated fatty acid (MUFA)s that are required for phospholipid and neutral lipid synthesis. Furthermore, blocking SCD‐1 increases saturated fatty acids like palmitate and stearate, which increase inflammation and insulin resistance. Thus, cultures of human adipocytes were treated with 50 uM 10,12 CLA and 30–300 uM oleic acid for 18–48 h. Consistent with our hypothesis, oleic acid reduced CLA‐mediated inflammatory gene expression in a dose‐dependent manner. However, oleic acid treatment did not attenuate CLA‐mediated insulin resistance. Notably, supplementation with stearic acid, a substrate for SCD‐1, or 9,11 CLA did not prevent inflammatory gene expression in 10,12 CLA‐treated cultures. Collectively, these data show that oleic acid attenuates CLA‐mediated inflammatory signaling, possibly by alleviating stress caused by SCD‐1 inhibition. Supported by NIH NIDDK‐ODS 5R01 DK063070‐09 and the UNCG URA program.