title: Exercise reverses metabolic syndrome in high-fat diet-induced obese rats.
abstract: OBJECTIVE
  Chronic consumption of a high-fat diet induces obesity. We investigated whether exercise would reverse the cardiometabolic disorders associated with obesity without it being necessary to change from a high- to normal-fat diet.
  
  
  METHODS
  Sprague-Dawley rats were placed on a high-fat (HFD) or control diet (CD) for 12 wk. HFD rats were then divided into four groups: sedentary HFD (HFD-S), exercise trained (motor treadmill for 12 wk) HFD (HFD-Ex), modified diet (HFD to CD; HF/CD-S), and exercise trained with modified diet (HF/CD-Ex). Cardiovascular risk parameters associated with metabolic syndrome were measured, and contents of aortic Akt, phospho-Akt at Ser (473), total endothelial nitric oxide synthase (eNOS), and phospho-eNOS at Ser (1177) were determined by Western blotting.
  
  
  RESULTS
  Chronic consumption of HFD induced a metabolic syndrome. Exercise and dietary modifications reduced adiposity, improved glucose and insulin levels and plasma lipid profile, and exerted an antihypertensive effect. Exercise was more effective than dietary modification in improving plasma levels of thiobarbituric acid-reacting substance and in correcting the endothelium-dependent relaxation to acetylcholine and insulin. Furthermore, independent of the diet used, exercise increased Akt and eNOS phosphorylation.
  
  
  CONCLUSIONS
  Metabolic syndrome induced by HFD is reversed by exercise and diet modification. It is demonstrated that exercise training induces these beneficial effects without the requirement for dietary modification, and these beneficial effects may be mediated by shear stress-induced Akt/eNOS pathway activation. Thus, exercise may be an effective strategy to reverse almost all the atherosclerotic risk factors linked to obesity, particularly in the vasculature.
authors.affiliation: UFR Sciences, Avignon, France. sabeur.touati@univ-avignon.fr
authors.forename: Sabeur
authors.initials: S
authors.lastname: Touati
authors.forename: Fayçal
authors.initials: F
authors.lastname: Meziri
authors.forename: Sylvie
authors.initials: S
authors.lastname: Devaux
authors.forename: Alain
authors.initials: A
authors.lastname: Berthelot
authors.forename: Rhian M
authors.initials: RM
authors.lastname: Touyz
authors.forename: Pascal
authors.initials: P
authors.lastname: Laurant
mesh_terms: D050154:Adiposity / Q000502:physiology; D000818:Animals; D001786:Blood Glucose / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D004032:Diet; D004041:Dietary Fats / Q000009:adverse effects*; D007328:Insulin / Q000097:blood; D008055:Lipids / Q000097:blood; D024821:Metabolic Syndrome / Q000209:etiology* / Q000628:therapy*; D052250:Nitric Oxide Synthase Type III / Q000502:physiology; D009765:Obesity / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051057:Proto-Oncogene Proteins c-akt / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D004041:Dietary Fats; D007328:Insulin; D008055:Lipids; D017392:Thiobarbituric Acid Reactive Substances; D052250:Nitric Oxide Synthase Type III; D051057:Proto-Oncogene Proteins c-akt