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禁食和重新喂食期间大鼠小肠胰岛素及胰岛素样生长因子I受体的比较

A comparison of rat small intestinal insulin and insulin-like growth factor I receptors during fasting and refeeding.

作者信息

Ziegler T R, Almahfouz A, Pedrini M T, Smith R J

机构信息

Joslin Research Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA.

出版信息

Endocrinology. 1995 Nov;136(11):5148-54. doi: 10.1210/endo.136.11.7588253.

DOI:10.1210/endo.136.11.7588253
PMID:7588253
Abstract

Insulin-like growth factor I (IGF-I) and insulin may be important regulators of intestinal growth. To investigate small intestinal IGF-I receptors (IGF-IR) and insulin receptors (IR) during intestinal cell atrophy and regeneration, we compared indexes of IGF-IR and IR expression in rat jejunum after 72 h of fasting and 24-72 h of enteral refeeding. Fasting induced intestinal atrophy, reduced plasma insulin and IGF-I concentrations, and markedly decreased jejunal IGF-I messenger RNA (mRNA) levels; these changes were reversed by refeeding. Fasting significantly increased jejunal specific insulin binding, IR content (to 230% of the fed control value), and the 9.6- and 7.4-kilobase IR mRNA transcript levels (to 202% and 218% of control values, respectively). These IR indexes rapidly decreased to control levels with refeeding. Levels of IGF-IR (by Scatchard analysis) and IGF-I-R mRNA were not significantly altered with fasting. The 11-kilobase IGF-IR mRNA transcript increased significantly during the first 24 h of refeeding (to 166% of the control value), and IGF-IR number rose 3-fold. We conclude that rat jejunal IR and IGF-IR are differentially regulated by nutrient availability. Up-regulation of jejunal IGF-I and IGF-IR expression during refeeding suggests a role for the IGF action pathway in gut trophic responses to enteral nutrients.

摘要

胰岛素样生长因子I(IGF-I)和胰岛素可能是肠道生长的重要调节因子。为了研究小肠细胞萎缩和再生过程中的小肠IGF-I受体(IGF-IR)和胰岛素受体(IR),我们比较了禁食72小时及肠内再喂养24 - 72小时后大鼠空肠中IGF-IR和IR表达的指标。禁食导致肠道萎缩,降低血浆胰岛素和IGF-I浓度,并显著降低空肠IGF-I信使核糖核酸(mRNA)水平;再喂养可逆转这些变化。禁食显著增加空肠特异性胰岛素结合、IR含量(达到喂食对照值的230%)以及9.6和7.4千碱基的IR mRNA转录水平(分别达到对照值的202%和218%)。随着再喂养,这些IR指标迅速降至对照水平。禁食时IGF-IR水平(通过Scatchard分析)和IGF-I-R mRNA没有显著改变。在再喂养的最初24小时内,11千碱基的IGF-IR mRNA转录本显著增加(达到对照值的166%),并且IGF-IR数量增加了3倍。我们得出结论,大鼠空肠IR和IGF-IR受营养可利用性的差异调节。再喂养期间空肠IGF-I和IGF-IR表达的上调表明IGF作用途径在肠道对肠内营养的营养反应中起作用。

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