Decreased liver fatty acid binding capacity and altered liver lipid distribution in mice lacking the liver fatty acid-binding protein gene.

摘要: Although liver fatty acid-binding protein (L-FABP) is an important binding site for various hydrophobic ligands in hepatocytes, its vivo significance not understood. We have therefore created L-FABP null mice and report here their initial analysis, focusing on the impact of this mutation hepatic acid capacity, lipid composition, expression other lipid-binding proteins. Gel-filtered cytosol from lacked main peak fraction that normally comprises both sterol carrier protein-2 (SCP-2). The capacity cis-parinaric was decreased >80% region. Molar ratios cholesterol/cholesterol ester, cholesteryl ester/triglyceride, cholesterol/phospholipid were 2- to 3-fold greater, reflecting up absolute increases specific classes order cholesterol > esters phospholipids. In contrast, pool sizes nonesterified acids triglycerides altered. However, deposition a bolus intravenously injected [14C]oleate markedly reduced, showing altered turnover. An increase ∼75% soluble SCP-2 but little or no change (glutathione S-transferase, albumin) membrane (fatty transport protein, CD36, aspartate aminotransferase, caveolin) transporters measured. These results (i) provide first time quantitative assessment contribution cytosolic (ii) establish as determinant composition turnover, (iii) suggest contributes accumulation liver.