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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >REGULATED EXPRESSION OF THE OBESE GENE PRODUCT (LEPTIN) IN WHITE ADIPOSE TISSUE AND 3T3-L1 ADIPOCYTES
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REGULATED EXPRESSION OF THE OBESE GENE PRODUCT (LEPTIN) IN WHITE ADIPOSE TISSUE AND 3T3-L1 ADIPOCYTES

机译：肥胖基因产物（瘦素）在白色脂肪组织和3T3-L1脂肪细胞中的调控表达

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A mutation within the obese gene was recently identified as the genetic basis for obesity in the ob/ob mouse, The obese gene product, leptin, is a 16-kDa protein expressed predominantly in adipose tissue, Consistent with leptin's postulated role as an extracellular signaling protein, human embryonic kidney 293 cells transfected with the obese gene secreted leptin with minimal intracellular accumulation. Upon differentiation of 3T3-L1 preadipocytes into adipocytes, the leptin mRNA aas expressed concomitant with mRNAs encoding adipocyte marker proteins, A factor(s) present in calf serum markedly activated expression of leptin by fully differentiated 3T3-L1 adipocytes. A 16-hr fast decreased (by approximate to 85%) the leptin mRNA level of adipose tissue of lean (ob/ + or +/+) mice but had no effect on the approximate to 4-fold higher level in obese (ob/ob) littermates. Since the mutation at the ob locus fails to produce the functional protein, yet its cognate mRNA is overproduced, it appears that leptin is necessary for its own downregulation, Leptin mRNA was also suppressed in adipose tissue of rats during a 16-hr fast and was rapidly induced during a 4-hr refeeding period. Insulin deficiency provoked by streptozotocin also markedly down-regulated leptin mRNA add this suppression was rapidly reversed by insulin, These results suggest that insulin may regulate the expression of leptin. [References: 29]
机译：肥胖基因中的突变最近被鉴定为肥胖症的遗传基础，肥胖基因产物瘦素是一种16kDa蛋白，主要在脂肪组织中表达，与瘦素作为细胞外信号传导的假定作用相一致肥胖基因转染的人类胚胎肾293细胞分泌的瘦素具有最小的细胞内积累。在将3T3-L1前脂肪细胞分化为脂肪细胞后，瘦素mRNA氨基酸表达与编码脂肪细胞标记蛋白的mRNA伴生，犊牛血清中存在的A因子通过完全分化的3T3-L1脂肪细胞显着激活了瘦素表达。瘦（ob / +或+ / +）小鼠脂肪组织的瘦素mRNA水平以16小时快速降低（大约为85％），但对肥胖者（ob / + / ob）同窝。由于在原位的突变无法产生功能性蛋白，但其同源mRNA却过量产生，因此瘦素似乎是其自身下调所必需的，在大鼠脂肪组织中，瘦素mRNA在禁食16小时的过程中也受到抑制，在4小时的喂食期间迅速诱发。链脲佐菌素引起的胰岛素缺乏也显着下调了瘦素mRNA，而这种抑制作用被胰岛素迅速逆转。这些结果表明，胰岛素可能调节了瘦素的表达。 [参考：29]

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