Journal
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
Volume 44, Issue 2, Pages 315-322Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2007.11.006
Keywords
fatty acids; hypertrophy; triacylglycerol; metabolism; heart failure
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Funding
- NHLBI NIH HHS [R01 HL062702-07, R37 HL049244-14, R01HL79415, R01 HL062702, R37HL049244, R01 HL079415-03, R37 HL049244, R01 HL079415, R01HL62702] Funding Source: Medline
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Intramyocardial lipid handling in pressure-overload-induced heart failure remains poorly understood, and the balance between endogenous and exogenous lipid utilization for mitochondrial ATP production is essentially unknown. In this study, we determined the contribution of endogenous triacylglycerols (TAG) to mitochondrial oxidation relative to that of exogenous palmitate, glucose, and endogenous glycogen in the failing, pressure-overloaded rat heart. TAG content and turnover were also assessed to determine if lipid availability and mobility were altered. Dynamic-mode C-13 NMR was performed in intact hearts from aortic banded and sham operated Spraque-Dawley rats perfused with C-13-labeled palmitate or glucose to assess TAG turnover rate and palmitate oxidation rate. The fractional contributions from palmitate, glucose, glycogen, and TAG to mitochondrial ATP production were determined from NMR analysis of heart extracts. TAG oxidation was not evident in HF, whereas the contribution of TAG to oxidative ATP production was significant in shams. TAG content was 39% lower in HF compared to sham, and TAG turnover rate was 60% lower in HE During adrenergic challenge, TAG sources were again not oxidized in the HF group. In early cardiac failure, endogenous TAG oxidation was reduced in parallel to increased carbohydrate oxidation, with no change in exogenous palmitate oxidation. This finding was consistent with reduced TAG storage and mobilization. These data further elucidate the role of intermediary and lipid metabolism in the progression of LVH to failure, and contribute to emerging evidence linking the disruption of myocardial substrate use to cardiomyopathies. (c) 2007 Elsevier Inc. All rights reserved.
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