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Liver fatty acid-binding protein and obesity Atshaves BP; Martin GG; Hostetler HA; McIntosh AL; Kier AB; Schroeder FJ Nutr Biochem 2010[Nov]; 21 (11): 1015-32While low levels of unesterified long chain fatty acids (LCFAs) are normal metabolic intermediates of dietary and endogenous fat, LCFAs are also potent regulators of key receptors/enzymes and at high levels become toxic detergents within the cell. Elevated levels of LCFAs are associated with diabetes, obesity and metabolic syndrome. Consequently, mammals evolved fatty acid-binding proteins (FABPs) that bind/sequester these potentially toxic free fatty acids in the cytosol and present them for rapid removal in oxidative (mitochondria, peroxisomes) or storage (endoplasmic reticulum, lipid droplets) organelles. Mammals have a large (15-member) family of FABPs with multiple members occurring within a single cell type. The first described FABP, liver-FABP (L-FABP or FABP1), is expressed in very high levels (2-5% of cytosolic protein) in liver as well as in intestine and kidney. Since L-FABP facilitates uptake and metabolism of LCFAs in vitro and in cultured cells, it was expected that abnormal function or loss of L-FABP would reduce hepatic LCFA uptake/oxidation and thereby increase LCFAs available for oxidation in muscle and/or storage in adipose. This prediction was confirmed in vitro with isolated liver slices and cultured primary hepatocytes from L-FABP gene-ablated mice. Despite unaltered food consumption when fed a control diet ad libitum, the L-FABP null mice exhibited age- and sex-dependent weight gain and increased fat tissue mass. The obese phenotype was exacerbated in L-FABP null mice pair fed a high-fat diet. Taken together with other findings, these data suggest that L-FABP could have an important role in preventing age- or diet-induced obesity.|Animals[MESH]|Cells, Cultured[MESH]|Diet[MESH]|Fatty Acid-Binding Proteins/genetics/*metabolism[MESH]|Fatty Acids/*metabolism[MESH]|Female[MESH]|Hepatocytes/metabolism[MESH]|Lipid Metabolism/*genetics[MESH]|Male[MESH]|Mice[MESH]|Mice, Inbred C57BL[MESH]|Mitochondria/metabolism[MESH]|Models, Biological[MESH]|Obesity/genetics/*metabolism[MESH]|Peroxisomes/metabolism[MESH]|Rats[MESH]|Weight Gain[MESH] |
