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胃肠外营养大鼠因肠切除及胰岛素样生长因子-I导致的空肠和结肠适应性差异

Differential jejunal and colonic adaptation due to resection and IGF-I in parenterally fed rats.

作者信息

Gillingham M B, Dahly E M, Carey H V, Clark M D, Kritsch K R, Ney D M

机构信息

Department of Nutritional Sciences, University of Wisconsin, Madison, Wisconsin 53706, USA.

出版信息

Am J Physiol Gastrointest Liver Physiol. 2000 May;278(5):G700-9. doi: 10.1152/ajpgi.2000.278.5.G700.

Abstract

Patients with severe short-bowel syndrome (SBS) often require long-term total parenteral nutrition (TPN) to maintain their nutritional status because of limited intestinal adaptation. Growth factors, including insulin-like growth factor I (IGF-I), are under investigation to promote intestinal adaptation and tolerance to oral feeding. We investigated structural and functional adaptation of the jejunum and colon in four groups of rats maintained with TPN for 7 days after a 60% jejunoileal resection and cecectomy or sham surgery and treatment with IGF-I or vehicle. Resection alone did not stimulate jejunal growth. IGF-I significantly increased jejunal mucosal mass, enterocyte proliferation, and migration rates. IGF-I decreased jejunal sucrase specific activity and reduced active ion transport and ionic permeability; resection alone had no effect. In contrast, resection significantly increased colonic mass and crypt depth but had no effect on active ion transport or ionic permeability. IGF-I had minimal effects on colonic structure. IGF-I but not resection stimulates jejunal adaptation, whereas resection but not IGF-I stimulates colonic growth in rats subjected to a model for human SBS. IGF-I treatment may improve intestinal adaptation in humans with SBS.

摘要

由于肠道适应性有限,严重短肠综合征(SBS)患者通常需要长期接受全胃肠外营养(TPN)以维持营养状况。包括胰岛素样生长因子I(IGF-I)在内的生长因子正在研究中,以促进肠道适应性和对口服喂养的耐受性。我们研究了四组大鼠空肠和结肠的结构和功能适应性,这些大鼠在60%空肠回肠切除和盲肠切除术后或假手术后接受TPN维持7天,并接受IGF-I或赋形剂治疗。单独切除不会刺激空肠生长。IGF-I显著增加空肠黏膜质量、肠上皮细胞增殖和迁移率。IGF-I降低空肠蔗糖酶比活性,减少主动离子转运和离子通透性;单独切除无影响。相比之下,切除显著增加结肠质量和隐窝深度,但对主动离子转运或离子通透性无影响。IGF-I对结肠结构影响极小。在人类SBS模型大鼠中,IGF-I而非切除刺激空肠适应性,而切除而非IGF-I刺激结肠生长。IGF-I治疗可能改善人类SBS患者的肠道适应性。

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