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Publication : Oleoylethanolamide differentially regulates glycerolipid synthesis and lipoprotein secretion in intestine and liver.

First Author  Pan X Year  2018
Journal  J Lipid Res Volume  59
Issue  12 Pages  2349-2359
PubMed ID  30369486 Mgi Jnum  J:269340
Mgi Id  MGI:6259964 Doi  10.1194/jlr.M089250
Citation  Pan X, et al. (2018) Oleoylethanolamide differentially regulates glycerolipid synthesis and lipoprotein secretion in intestine and liver. J Lipid Res 59(12):2349-2359
abstractText  Dietary fat absorption takes place in the intestine, and the liver mobilizes endogenous fat to other tissues by synthesizing lipoproteins that require apoB and microsomal triglyceride transfer protein (MTP). Dietary fat triggers the synthesis of oleoylethanolamide (OEA), a regulatory fatty acid that signals satiety to reduce food intake mainly by enhancing neural PPARalpha activity, in enterocytes. We explored OEA's roles in the assembly of lipoproteins in WT and Ppara (-/-) mouse enterocytes and hepatocytes, Caco-2 cells, and human liver-derived cells. In differentiated Caco-2 cells, OEA increased synthesis and secretion of triacylglycerols, apoB secretion in chylomicrons, and MTP expression in a dose-dependent manner. OEA also increased MTP activity and triacylglycerol secretion in WT and knockout primary enterocytes. In contrast to its intestinal cell effects, OEA reduced synthesis and secretion of triacylglycerols, apoB secretion, and MTP expression and activity in human hepatoma Huh-7 and HepG2 cells. Also, OEA reduced MTP expression and triacylglycerol secretion in WT, but not knockout, primary hepatocytes. These studies indicate differential effects of OEA on lipid synthesis and lipoprotein assembly: in enterocytes, OEA augments glycerolipid synthesis and lipoprotein assembly independent of PPARalpha. Conversely, in hepatocytes, OEA reduces MTP expression, glycerolipid synthesis, and lipoprotein secretion through PPARalpha-dependent mechanisms.
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