Lipid metabolism in heart and

LILIANA B. OLIVEROS, LAURA V. GATICA AND MAR¨ªA S.GIMENEZZ

Advances in Lipid Metabolism,

Research Signpost

Lugar: Kerala India; Año: 2008; p. 169 - 192

Abstract Retinoids, the naturally occurring and synthetic derivatives of vitamin A, modulate numerous fundamental physiological processes such as cellular differentiation, proliferation and apoptosis. The liver is the main storage site for vitamin A and also regulates the secretion of retinol into the circulation in response to the demands of target tissues. The molecular mechanism of retinoic acid action mainly involves the binding and activation of specific nuclear receptors, retinoic acid receptor (RAR) and retinoid X receptor (RXR) that modulate gene expression. The vitamin A metabolite, 9-cis retinoic acid, is the most potent ligand of RXR. Correspondence/Reprint request: Dra. Liliana Beatriz Oliveros, Fisiologia Humana, Departamento de Bioqu¨ªmica y Ciencias Biol¨®gicas, Universidad Nacional de San Luis Avenida Ej¨¦rcito de los Andes 950 CP 5700 - San Luis, Argentina. E-mail: lolive@unsl.edu.ar It is known that peroxisome proliferator-activated receptors (PPARs) form heterodimers with RXR to interact with a peroxisome proliferator responsive element of target gene and to regulate transcriptional expression. Natural fatty acids are ligands of PPARs, this fact, together with the function of identified target genes indicate that PPARs play a key role in lipid homeostasis. The lipoperoxidation induced by vitamin A deficiency has been communicated in several works. However, the molecular mechanisms underlying the many effects of retinoic acid on heart and aorta lipid metabolisms are not well understood. This chapter focuses on the vitamin A influencing cellular and molecular regulation of lipid metabolism in heart and aorta. In particular, the functions of PPAR ¦Á on energetic mitochondrial processes in cardiac tissue and the effects of oxidized LDL in aorta are discussed. and the effects of oxidized LDL in aorta are discussed. ¦Á on energetic mitochondrial processes in cardiac tissue and the effects of oxidized LDL in aorta are discussed.