title: Effects of exercise training on cardiac apoptosis in obese rats.
abstract: OBJECTIVE
  The purpose of this study was to evaluate the effects of exercise training on cardiac apoptotic pathways in obesity.
  
  
  RESULTS
  Sixteen lean Zucker rats (LZR) and sixteen obese Zucker rats (OZR) of 5-6 months of age as well as the other sixteen obese rats were subjected to treadmill running exercise for 1 h everyday for 3 months (OZR-EX). After exercise training or sedentary status of the rats, the excised hearts from the three groups were measured by heart weight index, H&E staining, TUNEL assays and Western blotting. Cardiac TUNEL-positive apoptotic cells, the protein levels of TNF alpha, Fas ligand, Fas receptors, Fas-associated death domain (FADD), Bad, Bax, activated caspase 8, activated caspase 9, and activated caspase 3 were higher in OZR than those in LZR. The protein levels of TNF alpha, Fas ligand, Fas receptors, FADD, activated caspase 8, and activated caspase 3 (Fas pathway) and the protein levels of Bad, Bax, Bax-to-Bcl2 ratio, activated caspase 9, and activated caspase 3 (mitochondria pathway) were lower in OZR-EX than those in OZR.
  
  
  CONCLUSIONS
  Cardiac Fas-dependent and mitochondria-dependent apoptotic pathways become more activated in obesity. Exercise training can prevent obesity-activated cardiac Fas-dependent and mitochondria-dependent apoptotic pathways. Our findings demonstrate a new therapeutic effect of exercise training to prevent delirious cardiac Fas-mediated and mitochondria-mediated apoptosis in obesity.
authors.affiliation: Department of Physical Therapy, Graduate Institute of Rehabilitation Science, China Medical University, Taichung, Taiwan.
authors.forename: S-D
authors.initials: SD
authors.lastname: Lee
authors.forename: W-C
authors.initials: WC
authors.lastname: Shyu
authors.forename: I-S
authors.initials: IS
authors.lastname: Cheng
authors.forename: C-H
authors.initials: CH
authors.lastname: Kuo
authors.forename: Y-S
authors.initials: YS
authors.lastname: Chan
authors.forename: Y-M
authors.initials: YM
authors.lastname: Lin
authors.forename: C-Y
authors.initials: CY
authors.lastname: Tasi
authors.forename: C-H
authors.initials: CH
authors.lastname: Tsai
authors.forename: T-J
authors.initials: TJ
authors.lastname: Ho
authors.forename: C-Y
authors.initials: CY
authors.lastname: Huang
mesh_terms: D000818:Animals; D017209:Apoptosis; D001794:Blood Pressure; D053148:Caspase 3 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D004452:Echocardiography; D053222:Fas Ligand Protein / Q000378:metabolism; D053200:Fas-Associated Death Domain Protein / Q000378:metabolism; D006321:Heart / Q000503:physiopathology*; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism; D009765:Obesity / Q000503:physiopathology*; D010805:Physical Conditioning, Animal; D051381:Rats; D011924:Rats, Zucker; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism; D019014:fas Receptor / Q000378:metabolism
chemical_list: C494828:Bax protein, rat; C505535:Fadd protein, rat; D053222:Fas Ligand Protein; D053200:Fas-Associated Death Domain Protein; D014409:Tumor Necrosis Factor-alpha; D051028:bcl-2-Associated X Protein; D019014:fas Receptor; C505410:Casp3 protein, rat; C506435:Casp9 protein, rat; D053148:Caspase 3; D053453:Caspase 9