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首页> 外文期刊>The Journal of Nutritional Biochemistry >Liver fatty acid-binding protein and obesity.
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Liver fatty acid-binding protein and obesity.

机译：肝脂肪酸结合蛋白与肥胖症有关。

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While 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.Digital Object Identifier http://dx.doi.org/10.1016/j.jnutbio.2010.01.005
机译：低水平的未酯化长链脂肪酸（LCFA）是膳食和内源性脂肪的正常代谢中间体，而LCFA也是关键受体/酶的有效调节剂，高水平时会成为细胞内的有毒清洁剂。 LCFA水平升高与糖尿病，肥胖症和代谢综合征相关。因此，哺乳动物进化出了脂肪酸结合蛋白（FABP），它们结合/隔离了细胞溶质中的这些潜在有毒的游离脂肪酸，并呈递给它们以在氧化（线粒体，过氧化物酶体）或储存（内质网，脂质滴）的细胞器中快速去除。哺乳动物有一个很大的FABP家族（15个成员），单个细胞类型中有多个成员。首先描述的FABP，肝脏FABP（L-FABP或FABP1）在肝脏以及肠和肾中都以很高的水平（2-5％的细胞溶质蛋白）表达。由于L-FABP促进体外和培养细胞中LCFA的摄取和代谢，因此预期功能异常或L-FABP丢失会降低肝LCFA摄取/氧化，从而增加可用于氧化的LCFA。在肌肉中和/或在脂肪中储存。体外分离的肝切片和L-FABP基因消融小鼠的原代肝细胞的培养证实了这一预测。尽管随意喂食对照饮食后食物摄入没有变化，但L-FABP无效小鼠表现出年龄和性别依赖性的体重增加和脂肪组织质量增加。喂高脂饮食的L-FABP空小鼠对肥胖表型加剧。结合其他发现，这些数据表明L-FABP可能在预防年龄或饮食引起的肥胖中起重要作用。数字对象标识符http://dx.doi.org/10.1016/j.jnutbio.2010.01.005

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