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Alpha linolenic acid increases cholesterol efflux via regulation of stearoyl CoA desaturase in foam cells
Author(s) -
Zhang Jun,
Vanden Heuvel John,
KrisEtherton Penny
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.724.17
Subject(s) - foam cell , efflux , lipogenesis , cholesterol , chemistry , abca1 , biochemistry , endocrinology , medicine , lipid metabolism , lipoprotein , biology , gene , transporter
Epidemiologic studies indicate that higher alpha linolenic acid (ALA) intake is associated with reduced cardiovascular disease risk. Stearoly CoA desaturase (SCD) is a rate‐limiting enzyme in lipogenesis by converting saturated fatty acids to monounsaturated fatty acids. Increased SCD activity is related with obesity, metabolic syndrome and atherosclerosis. There is some evidence that SCD1 also is involved in the cholesterol efflux from macrophage foam cells, important mediators of the atherogenic plaque. The current study was conducted to investigate the regulation of SCD1 by ALA and its contribution to cholesterol efflux. To induce foam cell formation, RAW 264.7 macrpohages were treated with oxidized low‐density lipoprotein (oxLDL). ALA treatment significantly decreased SCD1 mRNA expression by 88% in foam cells. ALA protein also was reduced by ALA treatment tested by western blot. In addition, ALA treatment induced a small yet significant increase of cholesterol efflux in foam cells. An increased cholesterol efflux also was observed in SCD1 knock down macrophage stable cell line. In overexpression SCD1 macrophage stable cell line, the cholesterol efflux was significantly decreased. We conclude that ALA increases cholesterol efflux via inhibition of SCD1 and would be beneficial to atherosclerosis regression via increasing efflux from lipid ladened foam cell.