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Obesity superimposed on aging magnifies the inflammatory and plasma lipid mediator responses following myocardial infarction (1155.1)
Author(s) -
Halade Ganesh,
Lopez Elizabeth,
Kabarowski Janusz,
Lindsey Merry
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.1155.1
Subject(s) - medicine , endocrinology , myocardial infarction , inflammation , obesity , arachidonic acid , myeloperoxidase , lipid signaling , diabetes mellitus , chemistry , biochemistry , enzyme
Fatty acids intake has increased over the last 100 years, contributing to an increase in obesity and diabetes. Obesity and aging are both risk factors for myocardial infarction (MI). How obesity interacts with aging to alter the post‐MI response, however, is unclear. We tested the hypothesis that obesity and aging would impair the resolution of post‐MI inflammation. Mice (12 month old C57BL/6J) fed with 10% (w/w) safflower oil (SO) diet for 5 months showed 28% higher fat mass than lean controls (LC). At 17 months of age, mice were subjected to coronary artery ligation to induce MI. At d1 post‐MI, infarct areas were 42±1% and 45±1% in SO and LC, respectively (p=n.s.). Obese mice showed higher neutrophil infiltration into the infarcted area and elevated VCAM‐1 levels compared to LC (both p<0.05). Plasma analysis revealed that monocyte chemotactic protein‐3, macrophage inflammatory protein‐1 and CD40 were increased at d1, while myeloperoxidase was increased at d5 post‐MI, in the SO group compared to LC (all p<0.05). Lipidomic analysis showed higher levels of arachidonic acid in SO group at all‐time points compared to LC (all p<0.05). Further, 12(S) Hydroxyeicosatetraenoic acid was increased at d1 compared to LC (p<0.05). Together, our results indicate that obesity accentuated the post‐MI inflammatory response by stimulating neutrophil trafficking and pro‐inflammatory lipid mediators.