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Title: Ligand specific variation in cardiac response to stimulation of peroxisome proliferator-activated receptor-alpha in spontaneously hypertensive rat
Authors: Ismael, S
Purushothaman, S
Harikrishnan, VS
Nair, RR
Keywords: Cell Biology
Issue Date: 2015
Citation: 406 ,42767;173-182
Abstract: Left ventricular hypertrophy (LVH) is an independent risk factor for cardiac failure. Reduction of LVH has beneficial effects on the heart. LVH is associated with shift in energy substrate preference from fatty acid to glucose, mediated by down regulation of peroxisome proliferator-activated receptor-alpha (PPAR-alpha). As long-term dependence on glucose can promote adverse cardiac remodeling, it was hypothesized that, prevention of metabolic shift by averting down regulation of PPAR-alpha can reduce cardiac remodeling in spontaneously hypertensive rat (SHR). Cardiac response to stimulation of PPAR-alpha presumably depends on the type of ligand used. Therefore, the study was carried out in SHR, using two different PPAR-alpha ligands. SHR were treated with either fenofibrate (100 mg/kg/day) or medium-chain triglyceride (MCT) Tricaprylin (5 % of diet) for 4 months. Expression of PPAR-alpha and medium-chain acylCoA dehydrogenase served as markers, for stimulation of PPAR-alpha. Both ligands stimulated PPAR-alpha. Decrease of blood pressure was observed only with fenofibrate. LVH was assessed from heart-weight/body weight ratio, histology and brain natriuretic peptide expression. As oxidative stress is linked with hypertrophy, serum and cardiac malondialdehyde and cardiac 3-nitrotyrosine levels were determined. Compared to untreated SHR, LVH and oxidative stress were lower on supplementation with MCT, but higher on treatment with fenofibrate. The observations indicate that reduction of blood pressure is not essentially accompanied by reduction of LVH, and that, progressive cardiac remodeling can be prevented with decrease in oxidative stress. Contrary to the notion that reactivation of PPAR-alpha is detrimental; the study substantiates that cardiac response to stimulation of PPAR-alpha is ligand specific.
URI: 10.1007/s11010-015-2435-x
Appears in Collections:Journal Articles

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