Maeda H, Kasahara K
Faculty of Health and Living Sciences, Naruto University of Education, Tokushima.
J Biochem. 1994 Jan;115(1):37-40. doi: 10.1093/oxfordjournals.jbchem.a124301.
The genetically obese Zucker rat is a well-characterized model of early-onset human obesity. The 120 kDa protein was recently found in the liver cytosol of obese Zucker rats at levels higher than that in lean Zucker rats. We isolated this protein using precipitation with ammonium sulfate, DEAE-Sephacel chromatography, and preparative polyacrylamide gel electrophoresis; the product showed a single band on SDS-polyacrylamide gel electrophoresis. Immunoblotting analysis revealed that the 120 kDa protein was predominantly localized in the liver cytosol of obese Zucker rats. The amount of this protein in lean Zucker rats was less than one-fifth of that found in obese Zucker rats. Further, there were only trace amounts of this protein in the lung tissues, and no detectable amount in other tissues, such as kidney, epididymal adipose tissue, brain, spleen, skeletal muscle, or serum, in either strain of rat. These data suggest that the 120 kDa protein contributes to the abnormal lipid metabolism in obese Zucker rats.
遗传性肥胖的 Zucker 大鼠是早发性人类肥胖的一种特征明确的模型。最近发现,肥胖 Zucker 大鼠肝胞质溶胶中的 120 kDa 蛋白水平高于瘦 Zucker 大鼠。我们使用硫酸铵沉淀、DEAE - 葡聚糖凝胶柱层析和制备型聚丙烯酰胺凝胶电泳分离了这种蛋白质;该产物在 SDS - 聚丙烯酰胺凝胶电泳上显示为单一条带。免疫印迹分析表明,120 kDa 蛋白主要定位于肥胖 Zucker 大鼠的肝胞质溶胶中。瘦 Zucker 大鼠中这种蛋白质的含量不到肥胖 Zucker 大鼠中所发现含量的五分之一。此外,在两种品系大鼠的肺组织中该蛋白含量仅为微量,而在其他组织如肾脏、附睾脂肪组织、脑、脾、骨骼肌或血清中均未检测到。这些数据表明,120 kDa 蛋白促成了肥胖 Zucker 大鼠异常的脂质代谢。