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磷酸盐缺乏会增加MDCK细胞中的IGF-II mRNA,但胰岛素样生长因子不参与磷酸盐转运对磷酸盐缺乏的适应性。

Deprivation of phosphate increases IGF-II mRNA in MDCK cells but IGFs are not involved in phosphate transport adaptation to phosphate deprivation.

作者信息

Ernest S, Coureau C, Escoubet B

机构信息

Institut National de la Santé et de la Recherche Médicale U 251, Faculté de Médecine Xavier Bichat, Université Denis Diderot Paris, France.

出版信息

J Endocrinol. 1995 May;145(2):325-31. doi: 10.1677/joe.0.1450325.

Abstract

Phosphate (Pi) deprivation and IGFs stimulate renal Pi reabsorption. We studied the involvement of IGFs in the adaptation of Pi transport to Pi deprivation in MDCK cells. Deprivation of Pi for 15 h increased the steady-state content of IGF-II mRNA (77 +/- 12%) whereas IGF-I mRNA was not detectable in MDCK cells in either control or Pi-deprived cells. IGF-II (10(-7) M) and IGF-I (10(-8) M) stimulated the Na-dependent Pi uptake (1.23- and 1.3-fold increase at 15 h respectively). The effect of IGF-I appeared after 15 h and increased up to 40 h of treatment (2.15-fold increase). In contrast, Pi uptake was increased by Pi deprivation as early as 8 h (1.5-fold) and up to 40 h of Pi deprivation (1.9-fold increase). IGF-II mRNA was not increased before 15 h of Pi deprivation and returned to control at 40 h. The combination of IGF-I and Pi deprivation had a more than additive effect on Pi transport (fivefold increase) (P < 0.001). At variance with Pi deprivation, high concentrations of insulin stimulated Na-coupled alanine transport (6 +/- 2% and 16 +/- 4% in Pi-treated and Pi-depleted cells respectively). Pi deprivation and high concentrations of insulin decreased Na,K-ATPase activity (-48 and -64% respectively) and these effects were not additive.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

磷酸盐(Pi)缺乏和胰岛素样生长因子(IGFs)可刺激肾脏对Pi的重吸收。我们研究了IGFs在MDCK细胞中Pi转运适应Pi缺乏过程中的作用。Pi缺乏15小时可使IGF-II mRNA的稳态含量增加(77±12%),而在对照或Pi缺乏的MDCK细胞中均未检测到IGF-I mRNA。IGF-II(10⁻⁷ M)和IGF-I(10⁻⁸ M)刺激了钠依赖性Pi摄取(分别在15小时时增加1.23倍和1.3倍)。IGF-I的作用在15小时后出现,并在处理40小时时增加(增加2.15倍)。相比之下,Pi缺乏早在8小时就使Pi摄取增加(1.5倍),并在Pi缺乏40小时时达到最大值(增加1.9倍)。Pi缺乏15小时之前IGF-II mRNA未增加,并在40小时时恢复到对照水平。IGF-I与Pi缺乏联合对Pi转运具有超相加效应(增加五倍)(P<0.001)。与Pi缺乏不同,高浓度胰岛素刺激钠偶联的丙氨酸转运(在Pi处理和Pi缺乏的细胞中分别增加6±2%和16±4%)。Pi缺乏和高浓度胰岛素降低了钠钾ATP酶活性(分别降低48%和64%),且这些效应无相加性。(摘要截短于250字)

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