Considine R V, Considine E L, Williams C J, Nyce M R, Magosin S A, Bauer T L, Rosato E L, Colberg J, Caro J F
Department of Medicine, Jefferson Medical College of Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
J Clin Invest. 1995 Jun;95(6):2986-8. doi: 10.1172/JCI118007.
Obese (ob) gene expression in abdominal subcutaneous adipocytes from lean and obese humans was examined. The full coding region of the ob gene was isolated from a human adipocyte cDNA library. Translation of the insert confirmed the reported amino acid sequence. There was no difference in the sequence of an reverse transcription PCR product of the coding region from five lean and five obese subjects. The nonsense mutation in the ob mouse which results in the conversion of arginine 105 to a stop codon was not present in human obesity. In all 10 human cDNAs, arginine 105 was encoded by CGG, consequently two nucleotide substitutions would be required to result in a stop codon. To compare the amount of ob gene expression in lean and obese individuals, radiolabed primer was used in the PCR reaction with beta-actin as a control. There was 72% more ob gene expression (P < 0.01) in eight obese subjects (body mass index, BMI = 42.8 +/- 2.7) compared to eight lean controls (BMI = 22.4 +/- 0.8). Regression analysis indicated a positive correlation between BMI and the amount of ob message (P < 0.005). There was no difference in the amount of beta-actin expression in the two groups. These results provide evidence that ob gene expression is increased in human obesity; furthermore, the mutations present in the mouse ob gene were not detected in the human mRNA population.
研究了瘦人和肥胖者腹部皮下脂肪细胞中肥胖（ob）基因的表达。从人脂肪细胞cDNA文库中分离出ob基因的完整编码区。插入片段的翻译证实了报道的氨基酸序列。来自五名瘦人和五名肥胖受试者的编码区逆转录PCR产物序列没有差异。人类肥胖中不存在ob小鼠导致精氨酸105转变为终止密码子的无义突变。在所有10个人类cDNA中，精氨酸105由CGG编码，因此需要两个核苷酸替换才能产生终止密码子。为了比较瘦人和肥胖个体中ob基因的表达量，在PCR反应中使用放射性标记引物，并以β-肌动蛋白作为对照。与八名瘦人对照组（BMI = 22.4 +/- 0.8）相比，八名肥胖受试者（体重指数，BMI = 42.8 +/- 2.7）的ob基因表达量高72%（P < 0.01）。回归分析表明BMI与ob信息的量呈正相关（P < 0.005）。两组中β-肌动蛋白的表达量没有差异。这些结果提供了证据表明人类肥胖中ob基因表达增加；此外，在人类mRNA群体中未检测到小鼠ob基因中存在的突变。
