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首页> 外文期刊>American Journal of Physiology >Intestinotrophic effects of exogenous IGF-I are not diminished in IGF binding protein-5 knockout mice.
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Intestinotrophic effects of exogenous IGF-I are not diminished in IGF binding protein-5 knockout mice.

机译：在IGF结合蛋白-5基因敲除小鼠中，外源性IGF-1的肠营养作用并未减弱。

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摘要

IGF binding protein-5 (IGFBP-5) modulates the availability of IGF-I to its receptor and potentiates the intestinotrophic action of IGF-I. Our aim was to test the hypothesis that stimulation of intestinal growth due to coinfusion of IGF-I with total parenteral nutrition (TPN) solution is dependent on increased expression of IGFBP-5 through conducting our studies in IGFBP-5 knockout (KO) mice. IGFBP-5 KO, heterozygote (HT) and wild type (WT) male and female mice were maintained with TPN or TPN plus coinfusion of IGF-I [recombinant human (rh)IGF-I; 2.5 mg x kg(-1) x day(-1)] for 5 days. The concentration of IGF-I in serum was 73% greater (P < 0.0001) in mice given TPN + IGF-I infusion compared with TPN alone. IGF-I attenuated the 2-3 g loss of body weight associated with TPN in WT mice, whereas KO and HT mice did not show improvement in body weight with IGF-I treatment. KO and HT mice had significantly greater levels of circulating IGF-I binding proteins (IGFBPs) compared with WT mice. Intestinal growth due to IGF-I was observed in all groups treated with IGF-I based on greater concentrations of protein and DNA in small intestine and colon and significantly greater crypt depth and muscularis thickness in jejunum. Jejunal expression of IGFBP-5 mRNA was greater in WT mice, whereas IGFBP-3 mRNA was greater in KO mice treated with IGF-I. In summary, the absence of the IGFBP-5 gene did not block the ability of IGF-I to stimulate intestinal growth, possibly because greater jejunal expression of IGFBP-3 compensates for the absence of IGFBP-5.
机译：IGF结合蛋白5（IGFBP-5）调节了IGF-1对其受体的利用，并增强了IGF-1的肠道营养作用。我们的目的是通过在IGFBP-5敲除（KO）小鼠中进行研究来检验以下假说：由于将IGF-1与全胃肠外营养（TPN）溶液共融合而刺激肠道生长取决于IGFBP-5表达的增加。用TPN或TPN加上IGF-1 [重组人（rh）IGF-1的共融合]维持IGFBP-5 KO，杂合子（HT）和野生型（WT）雄性和雌性小鼠。 2.5 mg x kg（-1）x day（-1）] 5天。与单独使用TPN相比，接受TPN + IGF-1输注的小鼠血清中IGF-1的浓度高73％（P <0.0001）。 IGF-1减轻了WT小鼠中与TPN有关的2-3g体重减轻，而KO和HT小鼠未显示出用IGF-1治疗的体重改善。与WT小鼠相比，KO和HT小鼠的循环IGF-1结合蛋白（IGFBPs）水平明显更高。基于小肠和结肠中较高的蛋白质和DNA浓度以及空肠中隐窝深度和肌层厚度明显较高，在所有用IGF-I治疗的组中均观察到了因IGF-I引起的肠生长。在WT小鼠中，IGFBP-5mRNA的空肠表达更高，而在用IGF-1处理的KO小鼠中，IGFBP-3mRNA更高。总之，IGFBP-5基因的缺失不会阻止IGF-1刺激肠道生长的能力，这可能是因为IGFBP-3的空肠表达增强弥补了IGFBP-5的缺失。

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