title: Chronic aerobic exercise associated to dietary modification improve endothelial function and eNOS expression in high fat fed hamsters.
abstract: Obesity is epidemic in the western world and central adipose tissue deposition points to increased cardiovascular morbidity and mortality, independently of any association between obesity and other cardiovascular risk factors. Physical exercise has been used as non-pharmacological treatment to significantly reverse/attenuate obesity comorbidities. In this study we have investigated effects of exercise and/or dietary modification on microcirculatory function, body composition, serum glucose, iNOS and eNOS expression on 120 male hamsters treated for 12 weeks with high fat chow (HF, n = 30) starting on the 21st day of birth. From week 12 to 20, animals were randomly separated in HF (no treatment change), return to standard chow (HFSC, n = 30), high fat chow associated to an aerobic exercise training program (AET) (HFEX, n = 30) and return to standard chow+AET (HFSCEX, n = 30). Microvascular reactivity in response to acetylcholine and sodium nitroprusside and macromolecular permeability increase induced by 30 minutes ischemia followed by reperfusion were assessed on the cheek pouch preparation. Total body fat and aorta eNOS and iNOS expression by immunoblotting assay were evaluated on the experimental day. Compared to HFSC and HFSCEX groups, HF and HFEX ones presented increased visceral fat [(mean±SEM) (HF)4.9±1.5 g and (HFEX)4.7±0.9 g vs. (HFSC)*3.0±0.7 g and (HFSCEX)*1.9±0.4 g/100 g BW]; impaired endothelial-dependent vasodilatation [Ach 10(-8) M (HF)87.9±2.7%; (HFSC)*116.7±5.9%; (HFEX)*109.1±4.6%; (HFSCEX)*105±2.8%; Ach10(-6) M (HF)95.3±3.1%; (HFSC)*126±6.2%; (HFEX)*122.5±2.8%; (HFSCEX)*118.1±4.3% and Ach10(-4) M (HF)109.5±4.8%; (HFSC)*149.6±6.6%; (HFEX)*143.5±5.4% and (HFSCEX)*139.4±5.2%], macromolecular permeability increase after ischemia/reperfusion [(HF)40.5±4.2; (HFSC)*19.0±1.6; (HFEX)*18.6±2.1 and (HFSCEX)* 21.5±3.7 leaks/cm2), decreased eNOS expression, increased leptin and glycaemic levels. Endothelial-independent microvascular reactivity was similar between groups, suggesting that only endothelial damage had occurred. Our results indicate that an aerobic routine and/or dietary modification may cause significant improvements to high fat fed animals, diminishing visceral depots, increasing eNOS expression and reducing microcirculatory dysfunction.
authors.affiliation: Laboratory for Clinical and Experimental Research on Vascular Biology (BioVasc), Biomedical Center, State University of Rio de Janeiro - Rio de Janeiro, RJ - Brazil.
authors.forename: Beatriz C S
authors.initials: BC
authors.lastname: Boa
authors.affiliation: Laboratory for Clinical and Experimental Research on Vascular Biology (BioVasc), Biomedical Center, State University of Rio de Janeiro - Rio de Janeiro, RJ - Brazil.
authors.forename: Maria das Graças C
authors.initials: Md
authors.lastname: Souza
authors.affiliation: Laboratory for Clinical and Experimental Research on Vascular Biology (BioVasc), Biomedical Center, State University of Rio de Janeiro - Rio de Janeiro, RJ - Brazil.
authors.forename: Richard D
authors.initials: RD
authors.lastname: Leite
authors.affiliation: Department of Cell Biology, Institute of Biology Roberto Alcântara Gomes, Biomedical Center, State University of Rio de Janeiro - Rio de Janeiro, RJ - Brazil.
authors.forename: Simone V
authors.initials: SV
authors.lastname: da Silva
authors.affiliation: Department of Cell Biology, Institute of Biology Roberto Alcântara Gomes, Biomedical Center, State University of Rio de Janeiro - Rio de Janeiro, RJ - Brazil.
authors.forename: Thereza Christina
authors.initials: TC
authors.lastname: Barja-Fidalgo
authors.affiliation: Laboratory for Clinical and Experimental Research on Vascular Biology (BioVasc), Biomedical Center, State University of Rio de Janeiro - Rio de Janeiro, RJ - Brazil; Department of Internal Medicine, Faculty of Medical Sciences, Biomedical Center, State University of Rio de Janeiro - Rio de Janeiro, RJ - Brazil.
authors.forename: Luiz Guilherme
authors.initials: LG
authors.lastname: Kraemer-Aguiar
authors.affiliation: Laboratory for Clinical and Experimental Research on Vascular Biology (BioVasc), Biomedical Center, State University of Rio de Janeiro - Rio de Janeiro, RJ - Brazil.
authors.forename: Eliete
authors.initials: E
authors.lastname: Bouskela
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000821:Animal Feed; D000818:Animals; D001013:Aorta, Thoracic / Q000737:chemistry; D001160:Arterioles / Q000187:drug effects / Q000502:physiology; D006224:Cricetinae; D004041:Dietary Fats / Q000633:toxicity*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism*; D004790:Enzyme Induction; D020738:Leptin / Q000097:blood; D008055:Lipids / Q000097:blood; D008297:Male; D008647:Mesocricetus; D008833:Microcirculation / Q000187:drug effects; D009061:Mouth Mucosa / Q000098:blood supply; D052250:Nitric Oxide Synthase Type III / Q000096:biosynthesis* / Q000235:genetics; D009599:Nitroprusside / Q000494:pharmacology; D010805:Physical Conditioning, Animal; D011897:Random Allocation; D014666:Vasomotor System / Q000187:drug effects / Q000502:physiology
chemical_list: D004041:Dietary Fats; D020738:Leptin; D008055:Lipids; D009599:Nitroprusside; D052250:Nitric Oxide Synthase Type III; D000109:Acetylcholine