![]() Conversely, a diet rich in unsaturated fatty acids has been suggested to reduce plasma triglycerides, cardiac arrhythmias, sudden death, risk of ischemic heart disease and heart failure, and is therefore recommended to improve cardiovascular health. The inconsistency in the data may be a consequence of several factors including: differences in the experimental models, dietary composition of the high fat diets utilized in the study, the time of initiation and duration of treatment, and the outcome measures analyzed.Ĭloser inspection of the literature reveals that in rodent models of left ventricular (LV) hypertrophy/dysfunction induced by pressure-overload, myocardial infarction, or sodium intake, most studies employed diets that were predominantly high in saturated fatty acids. In addition, cardiac function may be improved, impaired, or similar to chow fed animals. These studies have suggested that lipid metabolic pathways may be improved following high fat diet administration but pathological remodeling remains unaffected or attenuated. However, previous studies using various high fat diets in animal models have yielded mixed results. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Ĭompeting interests: The authors have declared that no competing interests exist.īased on epidemiological evidence demonstrating reduced cardiovascular risk and mortality with consumption of diets high in unsaturated fatty acids, dietary intervention strategies remain an attractive therapeutic option to combat the metabolic and cardiac remodeling processes that occur in the hypertrophied heart. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.ĭata Availability: All relevant data are within the paper and its Supporting Information files.įunding: This work was supported by the American Heart Association (14SDG18590020 to SCK) and the São Paulo Research Foundation (2012/19679-0 2014/06030-1 to LCT). Received: OctoAccepted: JanuPublished: March 1, 2018Ĭopyright: © 2018 Casquel De Tomasi et al. PLoS ONE 13(3):Įditor: Sudhiranjan Gupta, Texas A&M University Health Sciences Center, UNITED STATES (2018) Pathological hypertrophy and cardiac dysfunction are linked to aberrant endogenous unsaturated fatty acid metabolism. The HUFA diet is insufficient to reverse metabolic remodeling, diastolic dysfunction, or pathologically hypertrophy, possibly do to preferentially partitioning of unsaturated fatty acids to adipose tissue.Ĭitation: Casquel De Tomasi L, Salomé Campos DH, Grippa Sant’Ana P, Okoshi K, Padovani CR, Masahiro Murata G, et al. Overall, these results suggest that, in addition to decreased fatty acid oxidation, aberrant unsaturated fatty acid metabolism may be a maladaptive signature of the pathologically hypertrophied heart. The HUFA diet did not restore linoleate or oleate in the cardiac lipid pools, but did maintain body weight and adipose mass in SVAS animals. ![]() Mass spectrometry analysis revealed depletion of unsaturated fatty acids, primarily linoleate and oleate, within the endogenous lipid pools of normolipidic SVAS hearts. Enzymatic activity assays and gene expression analysis showed that both normolipidic and HUFA-fed hypertrophied hearts had similar increases in glycolytic enzyme activity and down-regulation of fatty acid oxidation genes. At 18 weeks post-surgery, the HUFA diet failed to normalize decreased E/A ratios or attenuate measures of cardiac hypertrophy in SVAS animals. After 6 weeks, diastolic dysfunction and pathological hypertrophy was confirmed and both sham and SVAS rats were treated with either normolipidic or HUFA diet. Male, Wistar rats were subjected to supra-valvar aortic stenosis (SVAS) or sham surgery. Since previous studies, using high saturated fat diets, have yielded inconclusive results, we investigated whether provision of a high-unsaturated fatty acid (HUFA) diet was sufficient to restore impaired lipid metabolism and normalize diastolic dysfunction in the pathologically hypertrophied heart. Pathological cardiac hypertrophy leads to derangements in lipid metabolism that may contribute to the development of cardiac dysfunction. ![]()
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