Baklanov A V, Bazhan N M
Ross Fiziol Zh Im I M Sechenova. 2015 Jun;101(6):689-99.
The relative gene expressions of glucose-6-phosphatase (G6P), phosphoenolpyruvate carbo- xykinase (PEPCK)--markers of gluconeogenesis, glucokinase (GK)--a marker of glycolysis, glucose transporter type 2 (GLUT2)--a marker of input and output of glucose in the liver were measured during the development of melanocortin (MC) obesity in male mice of C57BL/6J strain with mutation yellow in the Agouti locus (Ay/a mice). The mutation decreases MC receptor activity and induces hyperphagia and MC obesity. The males of the same line with mutation nonagouti were used as control. Tissue samples were taken at age 10 (before obesity), 15 (moderate obesity) and 30 (developed obesity) weeks. It has been shown that Ay/a mice had decreased glucose tolerance since 10-week age. There were age-related changes in mRNA levels in the liver of Ay/a mice, unlike a/a mice. In Ay/a mice the mRNA GLUT2 levels at the age of 10 weeks, mRNA GK levels at the age of 15 weeks, and mRNA G6P levels at the age of 3O weeks were higher than those in Ada mice of other ages. InAYfa mice the mRNA GK levels at the age of 15 weeks and mRNA G6F levels at the age of 30 weeks were increased relatively to those in a/a mice. Thus, Ay/a mice before the development of MK obesity had changes in the mRNA levels genes of proteins that regulate hepatic glucose metabolism, which may contribute to the compensation of glucose metabolism disorders caused by a hereditary decrease of MK system activity
在携带刺鼠基因座黄色突变的C57BL/6J品系雄性小鼠（Ay/a小鼠）黑素皮质素（MC）肥胖症发展过程中，检测了葡萄糖-6-磷酸酶（G6P）、磷酸烯醇式丙酮酸羧激酶（PEPCK）（糖异生标志物）、葡萄糖激酶（GK）（糖酵解标志物）、葡萄糖转运蛋白2型（GLUT2）（肝脏中葡萄糖输入和输出的标志物）的相对基因表达。该突变降低了MC受体活性，导致摄食亢进和MC肥胖症。将同一品系携带非刺鼠突变的雄性小鼠用作对照。在10周龄（肥胖前）、15周龄（中度肥胖）和30周龄（肥胖形成）时采集组织样本。结果表明，Ay/a小鼠从10周龄起葡萄糖耐量就降低。与a/a小鼠不同，Ay/a小鼠肝脏中的mRNA水平存在与年龄相关的变化。在Ay/a小鼠中，10周龄时的mRNA GLUT2水平、15周龄时的mRNA GK水平以及30周龄时的mRNA G6P水平均高于其他年龄的a/a小鼠。与a/a小鼠相比，Ay/a小鼠在15周龄时的mRNA GK水平和30周龄时的mRNA G6F水平相对升高。因此，在MC肥胖症形成之前，Ay/a小鼠调节肝脏葡萄糖代谢的蛋白质基因的mRNA水平发生了变化，这可能有助于补偿由MC系统活性遗传性降低引起的葡萄糖代谢紊乱。
