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High fat diet administration increases circulating 12‐hydroxyeicosatetraenoic acid levels in a mouse model of inflammatory disorders (LB535)
Author(s) -
Fung Victor,
Hough Greg
Publication year - 2014
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.28.1_supplement.lb535
Subject(s) - arachidonic acid , hydroxyeicosatetraenoic acid , inflammation , chemistry , endocrinology , medicine , docosahexaenoic acid , fatty acid , biochemistry , polyunsaturated fatty acid , biology , enzyme
12‐hydroperoxyeicosatetraenoic acid (12‐HPETE) is a product of oxidation of arachidonic acid (C20:4). HPETEs are prooxidant molecules that can lead to stimulation of several metabolic pathways resulting in an inflammatory condition in many organs. Fortunately our organism has evolved to use mechanisms to convert the potent 12‐HPETE to a lesser active molecule 12‐ hydroxyeicosatetraenoic acid, 12‐HETE. Still elevated levels of 12‐HETE are undesirable in most circumstances. We sought to determine the effect of a high fat diet in an animal model of inflammation namely ApoE deficient mouse. Methods: Three to four month old apoE deficient mice (n=20 per treatment group) were maintained on chow or Western type (WD) diet. After two weeks, the mice were fasted overnight and blood was removed, carefully protected from oxidative modification (addition of 20 uM BHT) and was cryopreserved. Using SepPak columns and a Q 4000 mass spectrometer, the plasma levels of 12‐HETE were determined. The data was analyzed using the software supplied by the manufacturer and statistical significance determined using ANOVA. Results: a high fat diet amplified the circulating levels of 12‐HETE which can activate pathways that produce inflammatory molecules. Conclusion: reducing fat consumption can lead to reduced level of plasma oxidized fatty acids which help alleviate the inflammatory pressure.