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首页> 外文期刊>Journal of Cellular Physiology >PTP1B deficiency enhances liver growth during suckling by increasing the expression of insulin-like growth factor-I.
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PTP1B deficiency enhances liver growth during suckling by increasing the expression of insulin-like growth factor-I.

机译：应用PTP1B缺乏肝脏的增长通过增加表达的吮吸胰岛素样生长因子。

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摘要

Protein tyrosine phosphatase 1B (PTP1B) is a negative regulator of insulin and tyrosine kinase growth factor signaling. We have recently demonstrated that PTP1B deficiency increases GLUT2/insulin receptor (IR) A complexes and glucose uptake in suckling, but not adult, primary hepatocytes. Herein we have investigated intrahepatic glucose utilization in 3-5 days old wild-type and PTP1B(-/-) mice. PTP1B deficiency decreased glycogen, lactate, and pyruvate content in the livers from suckling mice. Conversely, the activity of glucose 6-phosphate dehydrogenase (G6PD), the rate limiting enzyme of the pentose phosphate cycle (PPC) which provides substrates for DNA synthesis, was enhanced in the liver of PTP1B(-/-) animals. Liver weight, liver-to-body mass ratio, DNA content, and PCNA expression were increased in PTP1B(-/-) suckling mice compared to the wild-type controls. At the molecular level, STAT 5B phosphorylation, IGF-I mRNA, and protein levels as well as IGF-IR tyrosine phosphorylation were increased in the livers of PTP1B-deficient neonates. Unexpectedly, hepatic and serum triglycerides (TG) were increased by PTP1B deficiency, although the expression of lipogenic enzymes remained as in the wild-type controls. However, the analysis of milk composition revealed higher TG content in lactating females lacking PTP1B. The effects of PTP1B deficiency on G6PD activity, STAT 5B/IGF-I/IGF-IR axis, PCNA expression and liver growth during suckling were maintained by transferring PTP1B(-/-) embryos (PTP1B(-/-T)) to a wild-type female. Conversely, PTP1B(-/-T) mice did not show hepatic fat accumulation. In conclusion, the present study suggests that PTP1B plays a unique role in the control of the physiological liver development after birth.
机译：蛋白酪氨酸磷酸酶1 b(应用PTP1B)负调节胰岛素和酪氨酸激酶生长因子信号。表明应用PTP1B缺陷增加GLUT2 /胰岛素受体(IR)复合物在乳儿葡萄糖吸收,但不是成人,主要的肝细胞。肝内葡萄糖利用率在3 - 5天野生型和应用PTP1B(- / -)小鼠。糖原减少,乳酸和丙酮酸含量在乳儿的老鼠的肝脏。6-phosphate葡萄糖脱氢酶的活性(G6PD),限制酶的戊糖磷酸循环(PPC)提供基板对DNA合成,增强肝的应用PTP1B(- / -)动物。质量比、DNA含量和PCNA的表达增加应用PTP1B(- / -)幼鼠相比野生型的控制。统计5 b磷酸化、IGF-I信使rna和蛋白质以及IGF-IR酪氨酸磷酸化水平增加肝脏的PTP1B-deficient吗新生儿。甘油三酯(TG)增加了应用PTP1B不足,虽然脂肪生成的的表达酶仍在野生型控制。然而,牛奶成分的分析揭示高TG含量哺乳期女性缺乏应用PTP1B。G6PD活性,统计5 b / IGF-I IGF-IR轴,细胞核抗原表达和肝脏生长在吮吸由传输应用PTP1B(- / -)的胚胎(应用PTP1B (- / - t))野生型女性。应用PTP1B (- / - t)小鼠没有显示肝脂肪积累。表明应用PTP1B的过程中起着独特的作用肝脏的生理发展的控制出生后。

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