Myocardial Acot1 and other fatty acid-responsive genes were incre

Myocardial Acot1 and other fatty acid-responsive genes were increased to a lesser extent in WES diet-fed rats compared with high-fat fed animals, to which attenuated fatty acid oxidation and contractile dysfunction were attributed [62]. Expression of myocardial Acot1 is partly determined by ingested fatty acids, demonstrated in a study detailing the effect of a single dose of isolated fatty acids in mice [11]. More specifically, media enrichment with eicosapentaenoic Silmitasertib in vitro acid and DHA resulted in increased ACOT1 activity in cultured cells [63]. Consistent with this, increased Acot1 gene expression was measured in WES + DHA–fed

rats compared with CON animals, and similar directionality of protein expression was observed; this may represent an adaptive metabolic response underlying myocardial protection attributed to DHA. The family of Btg are studied primarily in relation to cancer, due to antiproliferative

effects attributable to cell cycle regulation [64] and [65]. B-cell translocation gene 2 has been detected in myocardial tissue in swine, where it appears to have a role in normal development [66]. Whether it plays a role in myocardial hypertrophy, where myocytes increase in size rather than number is unknown. In addition to effects on proliferation and development, BTG2 also protects human mammary epithelial cells from oxidative stress [67]. It is unknown whether BTG2 provides cardioprotection by a similar mechanism. Interestingly, Btg2 gene BKM120 purchase expression was decreased in WES + DHA rats compared with both CON and WES animals, and in the former comparison, similar trends in protein expression were observed. This suggests that the antiproliferative and oxidant protective effects attributed to BTG2 are not mechanisms of DHA-mediated cardioprotection. A comparison of myocardial gene expression relevant to adaptive and maladaptive hypertrophy was conducted using exercise-trained Interleukin-3 receptor and Dahl salt-sensitive rats, respectively.[8] At 6 months,

changes in heart weight and myocardial structure/function were more pronounced than in the present study. Compared with CON animals, Dahl salt-sensitive rats displayed differences in genes relevant to apoptosis, whereas exercise-trained animals displayed differences in genes associated with glucose and insulin regulation as well as protein synthesis. Genes known to be up-regulated with pathologic hypertrophy, atrial natriuretic factor, and brain natriuretic protein were also increased in the Dahl salt-sensitive rats. These trends were not observed in the present study, and relatively few genes in a given canonical or toxicologic pathway or biologic functional grouping were differentially expressed.

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