表皮生长因子对成年大鼠游离和总IGF-I及igf结合蛋白循环水平的影响。

Growth regulation Pub Date : 1996-03-01

J Frystyk, L Vinter-Jensen, C Skjaerbaek, A Flyvbjerg

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摘要

在新生大鼠中，全身给予表皮生长因子(EGF)导致体重增加减少和循环igf - 1水平降低，这表明它参与了表皮生长因子诱导的生长迟缓。我们研究了4周EGF给药对生理盐水(对照组)、30(低剂量组)和150(高剂量组)mg /kg/天EGF处理的成年大鼠循环游离和总IGF-I和igf结合蛋白(igfbp)的影响。用超滤液(游离)和酸乙醇提取物(总)测定血清igf - 1，用Western配体印迹法测定血清igfbp，得到四个不同的分子带。igfbp初步确定为IGFBP-3(42和38 kDa时的双带)、IGFBP-1和/或IGFBP-2 (30 kDa时的单带)和IGFBP-4 (24 kDa时的单带)。给药EGF没有改变体重、胫骨长度、肝脏、心脏和肺的重量。相比之下，血清总IGF-I和IGFBP-3呈剂量依赖性下降:总IGF-I平均为1470 +/- 100微克/升(对照组;平均+/- SEM)， 1030 +/- 60微克/升(低剂量组;P < 0.005)， 760 +/- 40微克/升(高剂量组;P < 0.005)，而IGFBP-3水平仅在对照组和高剂量大鼠之间有显著性差异(P < 0.05)。与对照组相比，低剂量组IGFBP-1和/或IGFBP-2水平升高(P < 0.05)，高剂量组无明显变化。IGFBP-4不受EGF影响。对照组的游离igf - 1平均为74 +/- 6微克/升，低剂量组降至35 +/- 6微克/升;P < 0.005)、57 +/- 5微克/升(高剂量组;P < 0.05)。游离igf -1与IGFBP-1和/或IGFBP-2呈负相关(r = -0.49, P < 0.05)。我们得出结论，在成年大鼠中，长期的EGF给药对循环中总igf - 1和游离igf - 1有明显的抑制作用。然而，我们没有观察到任何体细胞生长迟缓。

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The effect of epidermal growth factor on circulating levels of free and total IGF-I and IGF-binding proteins in adult rats.

In neonatal rats, systemic administration of epidermal growth factor (EGF) results in reduced body weight gain and decreased levels of circulating IGF-I, which suggests that it be involved in the EGF-induced growth retardation. We investigated the effect of 4 weeks of EGF administration on circulating free and total IGF-I and IGF-binding proteins (IGFBPs) in adult rats treated with saline (controls), 30 (low dose group) and 150 (high dose group) microgram/kg/day EGF. Serum IGF-I was determined in ultrafiltrates (free) and acid-ethanol extracts (total), and serum IGFBPs using Western ligand blotting, which yielded four distinct molecular bands. The IGFBPs were tentatively identified as IGFBP-3 (a double band at 42 and 38 kDa), IGFBP-1 and/or IGFBP-2 (a single band at 30 kDa) and IGFBP-4 (a single band at 24 kDa). EGF administration did not change the body weight, tibia length, or liver, heart and lung weight. In contrast, serum total IGF-I and IGFBP-3 decreased dose-dependently: total IGF-I averaged 1470 +/- 100 micrograms/l (controls; mean +/- SEM), 1030 +/- 60 micrograms/l (low dose group; P < 0.005) and 760 +/- 40 micrograms/l (high dose group; P < 0.005), whereas differences between IGFBP-3 levels reached significance (P < 0.05) between controls and high dose rats, only. When compared to controls, levels of IGFBP-1 and/or IGFBP-2 were increased in the low dose group (P < 0.05), but unchanged in the high dose group. IGFBP-4 was unaffected by EGF. Free IGF-I averaged 74 +/- 6 micrograms/l in controls, and was reduced to 35 +/- 6 micrograms/l (low dose group; P < 0.005) and 57 +/- 5 micrograms/l (high dose group; P < 0.05). Free IGF-I was inversely correlated (r = -0.49, P < 0.05) with IGFBP-1 and/or IGFBP-2. We conclude that in adult rats prolonged EGF administration has a marked depressing effect on circulating total and free IGF-I. Nevertheless, we did not observe any somatic growth retardation.

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Growth regulation

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