Epicardial fat gene expression after aerobic exercise training in pigs with coronary atherosclerosis: relationship to visceral and subcutaneous fat.
Epicardial adipose tissue (EAT) is contiguous with coronary arteries and myocardium and potentially may play a role in coronary atherosclerosis (CAD). Exercise is known to improve cardiovascular disease risk factors. The purpose of this study was to investigate the effect of aerobic exercise training on the expression of 18 genes, measured by RT-PCR and selected for their role in chronic inflammation, oxidative stress, and adipocyte metabolism, in peri-coronary epicardial (cEAT), peri-myocardial epicardial (mEAT), visceral abdominal (VAT), and subcutaneous (SAT) adipose tissues from a castrate male pig model of familial hypercholesterolemia with CAD. We tested the hypothesis that aerobic exercise training for 16 wk would reduce the inflammatory profile of mRNAs in both components of EAT and VAT but would have little effect on SAT. Exercise increased mEAT and total heart weights. EAT and heart weights were directly correlated. Compared with sedentary pigs matched for body weight to exercised animals, aerobic exercise training reduced the inflammatory response in mEAT but not cEAT, had no effect on inflammatory genes but preferentially decreased expression of adiponectin and other adipocyte-specific genes in VAT, and had no effect in SAT except that IL-6 mRNA went down and VEGFa mRNA went up. We conclude that 1) EAT is not homogeneous in its inflammatory response to aerobic exercise training, 2) cEAT around CAD remains proinflammatory after chronic exercise, 3) cEAT and VAT share similar inflammatory expression profiles but different metabolic mRNA responses to exercise, and 4) gene expression in SAT cannot be extrapolated to VAT and heart adipose tissues in exercise intervention studies.
Company
Joseph M
JM
Department of Biomedical Sciences, University of Missouri, Columbia, MO 65211, USA. jmc2gd@mizzou.edu
Booth
Frank W
FW
Laughlin
M Harold
MH
Arce-Esquivel
Arturo A
AA
Sacks
Harold S
HS
Bahouth
Suleiman W
SW
Fain
John N
JN
D054392:Adipokines / Q000235:genetics; D050154:Adiposity / Q000235:genetics*; D000818:Animals; D002369:Castration; D003324:Coronary Artery Disease / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D006938:Hyperlipoproteinemia Type II / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology; D007249:Inflammation / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D018836:Inflammation Mediators / Q000378:metabolism; D050152:Intra-Abdominal Fat / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D018384:Oxidative Stress / Q000235:genetics; D010496:Pericardium; D005082:Physical Exertion; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000378:metabolism; D050151:Subcutaneous Fat / Q000378:metabolism / Q000503:physiopathology*; D013552:Swine
D054392:Adipokines; D018836:Inflammation Mediators; D012333:RNA, Messenger