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生糖底物和神经内分泌因子对新生犊牛肝细胞
PEPCK-C mRNA表达水平的影响
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夏成1，王哲2，徐闯2，张洪友1，孙玉成2，王雪莹3
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（1.黑龙江八一农垦大学 动物科技学院，黑龙江 大庆163319； 2．吉林大学 畜牧兽医学院，吉林
长春130062； 3．吉林农业大学 动物科技学院，吉林 长春130118）
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摘要：
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在原代单层培养的新生犊牛肝细胞培养液中分别加入不同浓度丙酸钠、丙酮酸钠、胰岛素、胰高血糖素和瘦蛋白，培养12h后，应用半定量RT-PCR方法检测体外培养的肝细胞PEPCK-C mRNA的丰度。结果显示，随着丙酸钠、丙酮酸钠浓度的升高，肝细胞PEPCK-C mRNA的丰度均先升高后下降（P<0.01）；随胰岛素、胰高血糖素和瘦蛋白浓度的升高，肝细胞PEPCK-C mRNA的丰度分别剂量依赖性地降低、升高（P<0.01）和无显著变化。表明，丙酸钠、丙酮酸钠能通过上调体外培养的新生犊牛肝细胞PEPCK-C mRNA的表达而促进肝糖异生代谢，但上调作用是有限的；胰岛素能通过下调体外培养的新生犊牛肝细胞PEPCK-C mRNA的表达而抑制肝糖异生代谢，且下调作用呈剂量依赖性；胰高血糖素与胰岛素作用刚好相反；瘦蛋白未起直接的调节作用。 |
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关键词：
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生糖底物；神经内分泌因子；犊牛；肝细胞；PEPCK-C mRNA丰度 |
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中图分类号：Q 786 文献标识码：
A 文章编号：1673-4696(2006)04-0320-07 |
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Effects of substrates and neuroendocrine factors on expression of
PEPCK-C mRNA in neonatal calf hepatocytes in vitro |
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XIA Cheng1, WANG Zhe2, XU Chuang2, ZHANG
Hong-you1, SUN Yu-cheng2, WANG Xue-ying3 |
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（1.College of Animal Science and Technology, Heilongjiang August First Land Reclamation University, Daqing
163319,China; 2.College of Animal Science and Veterinary Medicine, Jilin University, Changchun 130062, China;
3. College of Animal Science and Technology, Jilin Agricultural University, Changchun 130118, China） |
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Abstract: Different concentrations of sodium propionate, sodium pyruvate, insulin, glucagons, and leptin were added respectively into monolayer culture media of primary-cultured calf hepatocytes. After the hepatocytes were cultured for 12h，abundance of PEPCK-C mRNA was detected by semiquantitative RT-PCR in primary-cultured calf hepatocytes.With increase of concentrations of sodium propionate or sodium pyruvate, the abundance of PEPCK-C mRNA in the hepatocytes increased significantly first, whereafter decreased. With increasing levels of insulin,glucagons, and leptin singly, the abundance of PEPCK-C mRNA in the hepatocyte dropped dose-dependently significantly, increased and had no difference, respectively. Sodium propionate and sodium pyruvate could promote liver gluconeogenesis by up-regulating the abundance of PEPCK-C mRNA in the hepatocytes, but the up-regulation was limited. Insulin could dose-dependently inhibit liver gluconeogenesis by down-regulating the abundance of PEPCK-C mRNA in the hepatocytes.The effect of glucagon was contrary to that of insulin. Leptin had no directly effect in regulating expression of PEPCK-C mRNA. |
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Key words: substrates; neuroendocrine factors; calf; hepatocytes; PEPCK-C mRNA expression |
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