Long-term treatment with the pan-PPAR agonist tetradecylthioacetic acid or fish oil is associated with increased cardiac content of n-3 fatty acids in rat

• Main Authors: Strand Elin, Bjorndal Bodil, Nygard Ottar, Burri Lena, Berge Christ, Bohov Pavol, Christensen Bjørn J, Berge Kjetil, Wergedahl Hege, Viste Asgaut, Berge Rolf K
• Format: Article
• Language: English
• Published: BMC 2012-06-01
• Series: Lipids in Health and Disease
• Subjects: Heart metabolism; Peroxisome proliferator-activated receptor; Polyunsaturated fatty acids; Tetradecylthioacetic acid
• Online Access: http://www.lipidworld.com/content/11/1/82

<p>Abstract</p> <p>Background</p> <p>Excess peroxisome proliferator-activated receptor (PPAR) stimulation has been associated with detrimental health effects including impaired myocardial function. Recently, supplementation with n-3 polyunsaturated fatty acids (PUFA) has been associated with improved left ventricular function and functional capacity in patients with dilated cardiomyopathy. We investigated the long-term effects of the pan-PPAR agonist tetradecylthioacetic acid (TTA) and/or high-dose fish oil (FO) on cardiac fatty acid (FA) composition and lipid metabolism. Male Wistar rats were given one out of four different 25% (w/v) fat diets: control diet; TTA diet; FO diet; or diet containing both TTA and FO.</p> <p>Results</p> <p>After 50 weeks n-3 PUFA levels were increased by TTA and FO in the heart, whereas liver levels were reduced following TTA administration. TTA was associated with a decrease in arachidonic acid, increased activities of carnitine palmitoyltransferase II, fatty acyl-CoA oxidase, glycerol-3-phosphate acyltransferase, and fatty acid synthase in the heart. Furthermore, cardiac <it>Ucp3</it> and <it>Cact</it> mRNA was upregulated.</p> <p>Conclusions</p> <p>Long-term treatment with the pan-PPAR agonist TTA or high-dose FO induced marked changes in PUFA composition and enzymatic activity involved in FA metabolism in the heart, different from liver. Changes included increased FA oxidation and a selective increase in cardiac n-3 PUFA.</p>