Growth hormone did not enhance mucosal hyperplasia after small-bowel resection

被引:35
作者
Park, JHY
Vanderhoof, JA
机构
[1] UNIV NEBRASKA, MED CTR, DEPT PEDIAT, OMAHA, NE USA
[2] CREIGHTON UNIV, OMAHA, NE 68178 USA
关键词
insulin-like growth factor-I; insulin-like growth factor binding proteins;
D O I
10.3109/00365529609006409
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background: Insulin-like growth factor (IGF)-I enhances the mucosal hyperplasia that normally occurs after massive small-bowel resection. The present studies examined whether growth hormone (GH) infusion increases serum IGF-I levels and, thereby, enhances mucosal hyperplasia after small-bowel resection. Methods: Male Sprague-Dawley rats weighing approximately 140 g were subjected to 80% jejunoileal resection or sham operation (ileal transection). A mini-osmotic pump was then inserted under the skin immediately after surgery to deliver either vehicle or 3 mg/kg/day GH. All animals were killed 7 days postoperatively, and the remaining intestine was removed and divided at the anastomotic site. Results: Food intake did not differ between control and GH-infused groups. Resected rats infused with GH grew faster than resected rats infused with vehicle. However, GH did not stimulate the weight gain of sham-operated rats. In both duodenojejunum and ileum, GH infusion did not stimulate hyperplasia beyond that which normally occurs after small-bowel resection, nor did it increase mucosal mass in sham-operated rats. GH infusion did not alter serum IGF-I or IGF-binding protein (IGFBP) levels in either resected or sham-operated rats. GH infusion resulted in increased sucrase and maltase activities in the ileal mucosa of resected rats. Conclusions: The present results suggest that a pharmacologic dose of GH directly stimulates growth of resected animals and heal sucrase and maltase activities without increasing serum IGF-I levels or increasing absorptive surface area in the small intestine.
引用
收藏
页码:349 / 354
页数:6
相关论文
共 46 条
[1]   DIVERGENT ILEAL IGF-I AND IGFBP-3 GENE-EXPRESSION AFTER SMALL-BOWEL RESECTION - A NOVEL MECHANISM TO AMPLIFY IGF ACTION [J].
ALBISTON, AL ;
TAYLOR, RG ;
HERINGTON, AC ;
BEVERIDGE, DJ ;
FULLER, PJ .
MOLECULAR AND CELLULAR ENDOCRINOLOGY, 1992, 83 (2-3) :R17-R20
[2]   THE SOMATOMEDINS - INSULIN-LIKE GROWTH-FACTORS [J].
BAXTER, RC .
ADVANCES IN CLINICAL CHEMISTRY, 1986, 25 :49-115
[3]   INSULIN-LIKE GROWTH FACTOR-I - A VALID NUTRITIONAL INDICATOR DURING PARENTERAL-FEEDING OF PATIENTS SUFFERING AN ACUTE PHASE RESPONSE [J].
BURGESS, EJ .
ANNALS OF CLINICAL BIOCHEMISTRY, 1992, 29 :137-144
[4]  
CLEMMONS DR, 1992, GROWTH REGULAT, V2, P80
[5]   USE OF PLASMA SOMATOMEDIN-C/INSULIN-LIKE GROWTH FACTOR-I MEASUREMENTS TO MONITOR THE RESPONSE TO NUTRITIONAL REPLETION IN MALNOURISHED PATIENTS [J].
CLEMMONS, DR ;
UNDERWOOD, LE ;
DICKERSON, RN ;
BROWN, RO ;
HAK, LJ ;
MACPHEE, RD ;
HEIZER, WD .
AMERICAN JOURNAL OF CLINICAL NUTRITION, 1985, 41 (02) :191-198
[6]   METHOD FOR ASSAY OF INTESTINAL DISACCHARIDASES [J].
DAHLQVIST, A .
ANALYTICAL BIOCHEMISTRY, 1964, 7 (01) :18-&
[7]   INSULIN-LIKE GROWTH FACTOR-I AND FACTOR-II - PEPTIDE, MESSENGER RIBONUCLEIC-ACID AND GENE STRUCTURES, SERUM, AND TISSUE CONCENTRATIONS [J].
DAUGHADAY, WH ;
ROTWEIN, P .
ENDOCRINE REVIEWS, 1989, 10 (01) :68-91
[8]   GROWTH-HORMONE (GH) STIMULATES INSULIN-LIKE GROWTH FACTOR-I (IGF-I) AND IGF-I-BINDING PROTEIN-3, BUT NOT GH RECEPTOR GENE-EXPRESSION IN LIVERS OF JUVENILE RATS [J].
DOMENE, H ;
KRISHNAMURTHI, K ;
ESHET, R ;
GILAD, I ;
LARON, Z ;
KOCH, I ;
STANNARD, B ;
CASSORLA, F ;
ROBERTS, CT ;
LEROITH, D .
ENDOCRINOLOGY, 1993, 133 (02) :675-682
[9]   AN IMPROVED DIPHENYLAMINE METHOD FOR ESTIMATION OF DEOXYRIBONUCLEIC ACID [J].
GILES, KW ;
MYERS, A .
NATURE, 1965, 206 (4979) :93-&
[10]   EFFECTS OF CONTINUOUS INFUSION OF INSULIN-LIKE GROWTH FACTOR-I AND FACTOR-II, ALONE AND IN COMBINATION WITH THYROXINE OR GROWTH-HORMONE, ON THE NEONATAL HYPOPHYSECTOMIZED RAT [J].
GLASSCOCK, GF ;
HEIN, AN ;
MILLER, JA ;
HINTZ, RL ;
ROSENFELD, RG .
ENDOCRINOLOGY, 1992, 130 (01) :203-210