title: High-fat diet prevents cardiac hypertrophy and improves contractile function in the hypertensive dahl salt-sensitive rat.
abstract: 1. The role that dietary lipid and plasma fatty acid concentration play in the development of cardiac hypertrophy in response to hypertension is not clear. 2. In the present study, we treated Dahl salt-sensitive rats with either normal chow (NC), normal chow with salt added (NC + salt) or a diet high in long-chain saturated fatty acids with added salt (HFD + salt). Cardiac function was assessed by echocardiography and left ventricular (LV) catheterization. 3. The HFD + salt group had significantly higher plasma free fatty acid concentrations and myocardial triglyceride content compared with the NC + salt group, but did not upregulate the activity of the fatty acid oxidation enzyme medium chain acyl-coenzyme A dehydrogenase. Systolic blood pressure was elevated to a similar extent in the NC + salt and HFD + salt groups compared with the NC group. Although LV mass was increased in the NC + salt group compared with the NC group, LV mass in the HFD + salt group did not differ from that of the NC group and was significantly lower than that in the NC + salt group. 4. There was no evidence of cardiac dysfunction in the NC + salt group compared with the NC group; however, high fat feeding significantly increased LV contractile performance (e.g. increased cardiac output and peak dP/dt). 5. In conclusion, the HFD + salt diet prevented the hypertrophic response to hypertension and improved the contractile performance of the heart. It remains to be determined whether preventing cardiac hypertrophic adaptations would be deleterious to the heart if the hypertensive stress is maintained long term.
authors.affiliation: Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio, USA.
authors.forename: Isidore C
authors.initials: IC
authors.lastname: Okere
authors.forename: David J
authors.initials: DJ
authors.lastname: Chess
authors.forename: Tracy A
authors.initials: TA
authors.lastname: McElfresh
authors.forename: Janean
authors.initials: J
authors.lastname: Johnson
authors.forename: Julie
authors.initials: J
authors.lastname: Rennison
authors.forename: Paul
authors.initials: P
authors.lastname: Ernsberger
authors.forename: Brian D
authors.initials: BD
authors.lastname: Hoit
authors.forename: Margaret P
authors.initials: MP
authors.lastname: Chandler
authors.forename: William C
authors.initials: WC
authors.lastname: Stanley
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D049628:Body Size / Q000187:drug effects; D006332:Cardiomegaly / Q000473:pathology / Q000517:prevention & control*; D004041:Dietary Fats / Q000008:administration & dosage / Q000494:pharmacology*; D004562:Electrocardiography; D005230:Fatty Acids, Nonesterified / Q000097:blood; D006352:Heart Ventricles / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D020303:Rats, Inbred Dahl; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage; D014280:Triglycerides / Q000097:blood / Q000378:metabolism
chemical_list: D004041:Dietary Fats; D005230:Fatty Acids, Nonesterified; D017673:Sodium Chloride, Dietary; D014280:Triglycerides