High-fat diet postinfarction enhances mitochondrial function and does not exacerbate left ventricular dysfunction.

High-fat diet postinfarction enhances mitochondrial function and does not exacerbate left ventricular dysfunction. Research Abstract Details 

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High-fat diet postinfarction enhances mitochondrial function and does not exacerbate left ventricular dysfunction. Abstract Text:

Julie H Rennison,Tracy A McElfresh,Isidore C Okere,Edwin J Vazquez,Hiral V Patel,Amy B Foster,Kalpana K Patel,Qun Chen,Brian D Hoit,Kou-Yi Tserng,Medhat O Hassan,Charles L Hoppel,Margaret P Chandler,

Lipid accumulation in nonadipose tissue due to enhanced circulating fatty acids may play a role in the pathophysiology of heart failure, obesity, and diabetes. Accumulation of myocardial lipids and related intermediates, e.g., ceramide, is associated with decreased contractile function, mitochondrial oxidative phosphorylation, and electron transport chain (ETC) complex activities. We tested the hypothesis that the progression of heart failure would be exacerbated by elevated myocardial lipids and an associated ceramide-induced inhibition of mitochondrial oxidative phosphorylation and ETC complex activities. Heart failure (HF) was induced by coronary artery ligation. Rats were then randomly assigned to either a normal (10% kcal from fat; HF, n = 8) or high saturated fat diet (60% kcal from saturated fat; HF + Sat, n = 7). Sham-operated animals (sham; n = 8) were fed a normal diet. Eight weeks postligation, left ventricular (LV) function was assessed by echocardiography and catheterization. Subsarcolemmal and interfibrillar mitochondria were isolated from the LV. Heart failure resulted in impaired LV contractile function [decreased percent fractional shortening and peak rate of LV pressure rise and fall (+/-dP/dt)] and remodeling (increased end-diastolic and end-systolic dimensions) in HF compared with sham. No further progression of LV dysfunction was evident in HF + Sat. Mitochondrial state 3 respiration was increased in HF + Sat compared with HF despite elevated myocardial ceramide. Activities of ETC complexes II and IV were elevated in HF + Sat compared with HF and sham. High saturated fat feeding following coronary artery ligation was associated with increased oxidative phosphorylation and ETC complex activities and did not adversely affect LV contractile function or remodeling, despite elevations in myocardial ceramide.

High-fat diet postinfarction enhances mitochondrial function and does not exacerbate left ventricular dysfunction. Publishing Authors By Initials

JH Rennison,TA McElfresh,IC Okere,EJ Vazquez,HV Patel,AB Foster,KK Patel,Q Chen,BD Hoit,KY Tserng,MO Hassan,CL Hoppel,MP Chandler,

For similar circulatory and respiratory physiology: cardiovascular physiology: cardiovascular physiologic processes: ventricular function: ventricular function, left research abstracts see: circulatory and respiratory physiology: cardiovascular physiology: cardiovascular physiologic processes: ventricular function: ventricular function, left research

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High-fat diet postinfarction enhances mitochondrial function and does not exacerbate left ventricular dysfunction. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: American journal of physiology. Heart and circulat

VOLUME: 292

Page Numbers: H1498-506

Journal Abbreviation: Am. J. Physiol. Heart Circ. Ph

ISSN: 0363-6135

DAY: 17

MONTH: 11

YEAR: 2006

High-fat diet postinfarction enhances mitochondrial function and does not exacerbate left ventricular dysfunction. Information

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LANGUAGE: eng

NlmUniqueID: 100901228

High-fat diet postinfarction enhances mitochondrial function and does not exacerbate left ventricular dysfunction. Keywords Mesh Terms:

KEYWORDS: Ventricular Function, Left

MESH TERMS: physiology

Chemical & Substance for Abstract: High-fat diet postinfarction enhances mitochondrial function and does not exacerbate left ventricular dysfunction. Information

Substance Name: Dietary Fats

Registry Number: 0

Grant and Affiliation Information for High-fat diet postinfarction enhances mitochondrial function and does not exacerbate left ventricular dysfunction.

AFFILIATION: Dept of Physiology and Biophysics, School of Medicine E558, Case Western Reserve Univ, Cleveland, OH 44106-4970, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: P01-HL-074237

ACRONYM: HL

MEDLINETA: Am J Physiol Heart Circ Physio

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