Abstract
Long-term dietary fatty acid intake alters the development of left ventricular hypertrophy, but the linking signaling pathways are unclear. We studied the role and underlying signaling mechanisms of dietary fat intake in the early phase of the hypertrophic process. Rats assigned for 4 weeks of high-oil, high-fat, or standard diet were subjected to angiotensin II (Ang II; 33 microg/kg/h, subcutaneous) or vehicle infusion for 24 h. The Ang II-induced increase in left ventricular mRNA levels of hypertrophy-associated genes was higher in rats fed the high-oil diet compared with the standard diet. Western blotting revealed that, in parallel with changes in gene expression, the high-oil diet increased c-Jun N-terminal kinase phosphorylation (P < 0.001). Ang II increased p38 mitogen-activated protein kinase (MAPK) phosphorylation in rats fed the high-fat diet (3-fold; P < 0.01). The increase in transcription factor activator protein-1 (AP-1) DNA binding activity in response to Ang II was higher in rats fed the high-oil diet compared with those fed the standard diet (P < 0.001). Ang II downregulated inducible nitric oxide synthase mRNA levels in fatty acid-supplemented groups compared with the standard diet group. These results show that dietary fat type modulates the early activation of hypertrophic genes in pressure-overloaded myocardium involving the distinct activation of AP-1 and MAPK signal transduction pathways.
Highlights
Long-term dietary fatty acid intake alters the development of left ventricular hypertrophy, but the linking signaling pathways are unclear
Given that fatty acids represent the main source of energy of hearts and that decreased fatty acid utilization has been suggested to play a role in the pathophysiology of cardiac hypertrophy [3], we hypothesized that dietary supplementation of fatty acids may influence the early hypertrophic process and activation of cardiac gene expression produced by pressure overload
The results presented here show that excess feeding of saturated or polyunsaturated fatty acids distinctly modified the expression of the hypertrophy-associated genes atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), and skeletal aactin in response to Ang angiotensin II (II)-induced pressure overload
Summary
Long-term dietary fatty acid intake alters the development of left ventricular hypertrophy, but the linking signaling pathways are unclear. The Ang II-induced increase in left ventricular mRNA levels of hypertrophy-associated genes was higher in rats fed the high-oil diet compared with the standard diet. Ang II downregulated inducible nitric oxide synthase mRNA levels in fatty acidsupplemented groups compared with the standard diet group These results show that dietary fat type modulates the early activation of hypertrophic genes in pressureoverloaded myocardium involving the distinct activation of AP-1 and MAPK signal transduction pathways.—Foldes, G., S. We measured left ventricular mRNA levels of the hypertrophy-associated genes atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), skeletal a-actin, and cfos in Ang II-induced pressure overload in rats randomly assigned to a standard, high-oil, or high-fat diet. The involvement of mitogen-activated protein kinases (MAPKs), c-Jun N-terminal protein kinases (JNKs), extracellular signal-regulated protein kinases (ERKs), and p38 kinase as well as transcription factor activator protein-1 (AP-1) and nuclear factor nB (NF-nB) DNA binding activity in the modulation of the hypertrophic process by dietary fat was characterized by immunoblotting and electrophoretic mobility shift analysis
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
