Differential Effects of in Vivo Ppar Α and Γ Activation on Fatty Acid Transport Proteins Expression and Lipid Content in Rat Liver

Long chain fatty acids (LCFAs) on their way from the microvascular compartment to the hepatocytes, first have to pass the capillary endothelium. As outlined in more details elsewhere, in the liver, unlike other tissues such as skeletal muscles or cardiac myocytes, the interendothelial clefts are abundantly present and allow the passage of the albumin-LCFA complexes (1). LCFAs are also present in the portal vein as a compound of chylomicrones, from which are released, and then traffic through the capillary endothelial cells via simple diffusion, according to their’s concentration gradient (2). However, recent years provided a considerable evidence to support the existence of a saturable, protein-mediated transport process for LCFAs into many tissues, including adipocytes (3, 4), intestine (5, 6), kidney (7), myocytes (8) and liver (9-11). Although controversy still exists as to the role of proteins in facilitating fatty acid uptake into hepatocytes, a recent study by Koonen at el. strongly supports the involvement of protein-mediated LCFA transport into the liver cells (12). Currently, at the transcriptional level, several proteins involved in facilitated fatty acid transport have been identified in the liver, including fatty acid translocase (FAT/CD36), plasma membrane associated fatty acid binding protein (FABPpm) and fatty acid transport proteins 1 and 5 (FATP1 and 5) (911). Among these, a key role for FAT/CD36 in the hepatic fatty acid transport had been proposed (12) as this appears to be a true for other metabolically JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY 2009, 60, 1, 99–106 www.jpp.krakow.pl