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Decreased Mitochondrial Respiratory Capacity does not correlate with Worsened LV Function in Heart Failure
Author(s) -
OConnell Kelly Anne,
Cox James,
Xu Wenhong,
Shekar Kadambari Chandra,
Gamble Dionna,
Woodman Bradley,
Stanley William C
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1192.3
Subject(s) - polyunsaturated fatty acid , medicine , mitochondrion , endocrinology , ejection fraction , heart failure , respiration , beta oxidation , cardiac function curve , chemistry , fatty acid , metabolism , biochemistry , anatomy
Nutritional therapies for heart failure (HF) are a potential adjunct to pharmaceutical interventions. High fat intake improves cardiac function in rodent models of HF. We compared a standard low fat diet (STD, 15% energy as fat) to diets high in monounsaturated fatty acids (MUFA, 18:1), n6‐polyunsaturated fatty acids (PUFA, 18:2n6) and long chain saturated fat (LCSat, 16:0 and 18:0) which contained 40% energy from fat. Rats were subjected to transverse aortic constriction (TAC) or sham surgery and randomized to dietary treatment after 10 weeks (n=16–17/group). After 16 weeks on diets, cardiac mitochondria were isolated. TAC increased LV mass by ~50% in all groups. LV ejection fraction decreased from 83±1% in sham to 48±5% with TAC on STD diet, 58±4% with MUFA, 56±3% with PUFA, but was prevented by LCSat (67±5%, P<0.05). Maximal mitochondrial respiration with palmitoylcarnitine was decreased from 194±23 to 113±13 nA O*mg −1 min −1 with TAC on STD diet and on PUFA (116±19 with TAC), but was prevented with MUFA and LCSat (169±19 and 168±19 nA O*mg −1 min −1 , respectively), consistent with PPARα activation and improved mitochondrial function. This suggests that increased capacity of fat oxidation does not cause an obligatory increase in LV function. LV function and the decline in mitochondrial capacity for fat oxidation are not causally linked, and impaired mitochondrial respiration does not predict LV remodeling in HF.