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Title

Triacylglycerol molecular species are depleted to different extents in the myocardium of spontaneously hypertensive rats fed two oleic acid-rich oils

AuthorsPerona, Javier S. ; Ruiz-Gutiérrez, Valentina
Issue DateJan-2005
PublisherNature Publishing Group
CitationAmerican Journal of Hypertension 18(1): 72-80 (2005)
AbstractBACKGROUND: During the development of hypertension, glucose replaces triacylglycerols (TG) as the main energy source for the myocardium. However, there are no available studies investigating the TG molecular species composition of the myocardium in the spontaneously hypertensive rat (SHR). The objective of this study was to evaluate the effect of two dietary oils (virgin olive oil [VOO] and high-oleic sunflower oil [HOSO]) with a similar oleic acid content but different TG moieties on lipid composition and especially on TG molecular species, and also the effect of on lipoprotein lipase (LPL) activity, on the SHR myocardium. METHODS: Wistar-Kyoto (WKY) rats and SHR were fed a baseline diet (BD) or a diet enriched by VOO or HOSO. Lipid classes, fatty acids of phospholipids (PL), TG, TG molecular species, and LPL were determined in the rat myocardium. RESULTS: We found a depletion of the TG pool in the myocardium of SHR, which was comcomitant with cardiac hypertrophy. The loss of this lipid class was not corrected by dietary administration and was due to a nonspecific reduction in the fatty acid content and a specific lowering of dilinoleoyl-acyl-glycerol and di-and tri-saturated TG species. In addition, we observed an increased accumulation of arachidonic acid (20:4, n-6) in the PL of the SHR group fed BD or HOSO but not in that fed VOO, as compared with the corresponding WKY. CONCLUSIONS: These results suggest that the depletion of TG in the heart of SHR is selective and is not reflected in the fatty acid profile. Although administration of either VOO or HOSO did not protect the heart against TG depletion, SHR fed VOO showed a more favorable PL compsition against changes caused by cardiac hypertrophy.
Publisher version (URL)http://dx.doi.org/10.1016/j.amjhyper.2004.11.012
URIhttp://hdl.handle.net/10261/55845
DOI10.1016/j.amjhyper.2004.11.012
ISSN0895-7061
E-ISSN1941-7225
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