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IMPACT OF HIGH FAT DIET ON MYOCARDIAL GENE EXPRESSION IN CARDIAC HYPERTROPHY
Author(s) -
Seymour AnneMarie L,
Akki Ashwin
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1409-a
Subject(s) - medicine , endocrinology , pdk4 , lipid metabolism , gene expression , pressure overload , muscle hypertrophy , cardiac function curve , beta oxidation , glut4 , ucp3 , carbohydrate metabolism , heart failure , chemistry , metabolism , cardiac hypertrophy , biology , diabetes mellitus , uncoupling protein , insulin resistance , gene , biochemistry , obesity , brown adipose tissue
Cardiac hypertrophy (CH) is characterised by metabolic remodelling, and a switch in substrate preference from fatty acids (FA) to glucose. Impaired FA oxidation, in the setting of CH, can result in an inappropriate accumulation of lipid, which may be an underlying cause of deterioration into decompensated heart failure. We therefore investigated alterations in gene expression of key metabolic enzymes involved in FA and glucose utilisation in CH in response to high fat feeding. Pressure‐overload hypertrophy was induced in male Sprague‐Dawley rats by abdominal aortic constriction (AC). Group‐1 received standard chow for 9 weeks whilst Group‐2 was fed a high‐fat diet (45% kcal from lipids) for 7 weeks from week 2. 9 weeks post‐surgery, gene expression was probed in control (Con) and AC hearts using real‐time PCR. CH was observed in AC vs. Con [Group 1, 0.66 ± 0.07∗ vs 0.54 ± 0.04; Group 2, 0.68 ± 0.09∗ vs 0.6 ± 0.06; ∗ p < 0.05]. In Group‐1, myocardial expression of PPAR∞ and PPARα‐regulated genes were significantly down‐regulated relative to Calsequestrin‐2 in AC vs. Con, consistent with our previous observation of a marked reduction in FA oxidation. In Group‐2, expression of PPAR∞, CPT1, MCAD and PDK4 normalised in AC, whilst UCP3 expression remained low. Thus, changes in expression and function of FA metabolism may contribute to functional deterioration in CH.