title: Body adiposity dictates different mechanisms of increased coronary reactivity related to improved in vivo cardiac function.
abstract: BACKGROUND
  Saturated fatty acid-rich high fat (HF) diets trigger abdominal adiposity, insulin resistance, type 2 diabetes and cardiac dysfunction. This study was aimed at evaluating the effects of nascent obesity on the cardiac function of animals fed a high-fat diet and at analyzing the mechanisms by which these alterations occurred at the level of coronary reserve.
  
  
  METHODS
  Rats were fed a control (C) or a HF diet containing high proportions of saturated fatty acids for 3 months. Thereafter, their cardiac function was evaluated in vivo using a pressure probe inserted into the cavity of the left ventricle. Their heart was isolated, perfused iso-volumetrically according to the Langendorff mode and the coronary reserve was evaluated by determining the endothelial-dependent (EDV) and endothelial-independent (EIV) vasodilatations in the absence and presence of endothelial nitric oxide synthase and cyclooxygenase inhibitors (L-NAME and indomethacin). The fatty acid composition of cardiac phospholipids was then evaluated.
  
  
  RESULTS
  Although all the HF-fed rats increased their abdominal adiposity, some of them did not gain body weight (HF- group) compared to the C group whereas other ones had a higher body weight (HF+). All HF rats displayed a higher in vivo cardiac activity associated with an increased EDV. In the HF- group, the improved EDV was due to an increase in the endothelial cell vasodilatation activity whereas in the HF+ group, the enhanced EDV resulted from an improved sensitivity of coronary smooth muscle cells to nitric oxide. Furthermore, in the HF- group the main pathway implicated in the EDV was the NOS pathway while in the HF+ group the COX pathway.
  
  
  CONCLUSIONS
  Nascent obesity-induced improvement of cardiac function may be supported by an enhanced coronary reserve occurring via different mechanisms. These mechanisms implicate either the endothelial cells activity or the smooth muscle cells sensitivity depending on the body adiposity of the animals.
authors.forename: Evangelia
authors.initials: E
authors.lastname: Mourmoura
authors.forename: Valérie
authors.initials: V
authors.lastname: Chaté
authors.forename: Karine
authors.initials: K
authors.lastname: Couturier
authors.forename: Brigitte
authors.initials: B
authors.lastname: Laillet
authors.forename: Guillaume
authors.initials: G
authors.lastname: Vial
authors.forename: Jean-Paul
authors.initials: JP
authors.lastname: Rigaudiere
authors.forename: Béatrice
authors.initials: B
authors.lastname: Morio
authors.forename: Corinne
authors.initials: C
authors.lastname: Malpuech-Brugère
authors.forename: Kasra
authors.initials: K
authors.lastname: Azarnoush
authors.affiliation: Université Joseph Fourier, Laboratoire de Bioénergétique Fondamentale et Appliquée, BP 53, Grenoble F-38041, France. luc.demaison@clermont.inra.fr.
authors.forename: Luc
authors.initials: L
authors.lastname: Demaison
mesh_terms: D050154:Adiposity / Q000502:physiology*; D000818:Animals; D003331:Coronary Vessels / Q000166:cytology / Q000502:physiology*; D059305:Diet, High-Fat / Q000009:adverse effects*; D008297:Male; D009765:Obesity / Q000378:metabolism / Q000503:physiopathology*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D014664:Vasodilation / Q000502:physiology*