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We began analyzing https://link.springer.com/article/10.1007/s11010-015-2435-x, but it redirected us to https://link.springer.com/article/10.1007/s11010-015-2435-x. The analysis below is for the second page.

Title[redir]:
Ligand specific variation in cardiac response to stimulation of peroxisome proliferator-activated receptor-alpha in spontaneously hypertensive rat | Molecular and Cellular Biochemistry
Description:
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-α). 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-α can reduce cardiac remodeling in spontaneously hypertensive rat (SHR). Cardiac response to stimulation of PPAR-α presumably depends on the type of ligand used. Therefore, the study was carried out in SHR, using two different PPAR-α 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-α and medium-chain acylCoA dehydrogenase served as markers, for stimulation of PPAR-α. Both ligands stimulated PPAR-α. 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-α is detrimental; the study substantiates that cardiac response to stimulation of PPAR-α is ligand specific.

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article, pubmed, google, scholar, cas, cardiac, heart, fenofibrate, rat, hypertrophy, peroxisome, proliferatoractivated, hypertensive, cell, spontaneously, pparα, mol, physiol, fatty, stress, hypertension, left, remodeling, oxidative, research, response, stimulation, receptoralpha, nair, ventricular, acid, metabolic, mediumchain, myocardial, central, alpha, purushothaman, lvh, failure, effects, blood, pressure, access, receptor, cardiol, pparalpha, rats, privacy, cookies, function,

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peroxisome proliferator-activated receptor-alpha peroxisome-proliferator-activated receptor alpha peroxisome proliferator-activated receptor-α peroxisome proliferator-activated receptor heart-weight/body weight ratio plant-derived fat high-fat feeding month download article/chapter porcine tachycardia-induced cardiomyopathy medium-chain fatty acids angiotensin ii-dependent hypertension medium-chain triglyceride therapy redox-regulated transcription factors medium-chain fatty acid real-time quantitative pcr preventing p65-nfκb binding pressure-overloaded rat hearts angiotensin ii-infused rats pparalpha activator fenofibrate medium-chain triglyceride normotensive wistar-kyoto rats ligands stimulated ppar-α related subjects laboratory animal sciences ligand specific variation blood pressure-independent attenuation left ventricular hypertrophy full article pdf fenofibrate prevents aldosterone-induced hypertension left ventricular mass ppar-alpha agonists left ventricular dysfunction privacy choices/manage cookies h1425–h1436 cellular biochemistry aims ppar-α ligands ppar-alpha agonist long-term dependence cardiac hypertrophic growth reduce cardiac remodeling progressive cardiac remodeling attenuates cardiac fibrosis senior research fellowship fatty acid oxidation article ismael spontaneously hypertensive rat hypertrophied rat heart independent risk factor article molecular

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Tanaka T, Sohmiya K, Kawamura K (1997) Is CD36 deficiency an etiology of hereditary hypertrophic cardiomyopathy?

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