Growth factors in inflammatory bowel disease - The actions and interactions of growth hormone and insulin-like growth factor-I

被引:55
作者
Theiss, AL [1 ]
Fruchtman, S [1 ]
Lund, PK [1 ]
机构
[1] Univ N Carolina, Dept Cell & Mol Physiol, Chapel Hill, NC 27599 USA
关键词
growth hormone; insulin-like growth factor-I; suppressors of cytokine signaling; fibrosis; cell proliferation;
D O I
10.1097/00054725-200411000-00021
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Multiple growth hormones (GHs) and factors arc relevant to inflammatory bowel disease (IBD) due to their trophic effects on epithelial cells to promote mucosal integrity, renewal, and repair, on mesenchymal cells to promote wound healing, and on intestinal immune cells to modulate inflammation. The anabolic effects of GHs and factors outside the intestine are relevant to minimizing nutritional insufficiency, catabolic state, and the inability to maintain body weight due to inflammation-induced malabsorption. GHs and factors can, however, have a dual role, whereby trophic effects can be beneficial but, if excessive, can promote complications including the increased risk of intestinal tumors/adenocarcinoma and fibrosis. This review focuses on GH and insulin-like growth factor (IGF-I), for which evidence suggests such a dual role may exist. The actions of GH and IGF-I on the healthy intestine are compared with effects during intestinal inflammation or associated complications. Interactions between these growth factors and others relevant to IBD are considered. The role of the newly discovered Suppressors of cytokine signaling proteins, which may dictate the balance between beneficial and excessive actions of GH and IGF-I, is also addressed.
引用
收藏
页码:871 / 880
页数:10
相关论文
共 127 条
[31]   Differential jejunal and colonic adaptation due to resection and IGF-I in parenterally fed rats [J].
Gillingham, MB ;
Dahly, EM ;
Carey, HV ;
Clark, MD ;
Kritsch, KR ;
Ney, DM .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2000, 278 (05) :G700-G709
[32]   IGF-I treatment facilitates transition from parenteral to enteral nutrition in rats with short bowel syndrome [J].
Gillingham, MB ;
Dahly, EM ;
Murali, SG ;
Ney, DM .
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 2003, 284 (02) :R363-R371
[33]   Insulin, insulin-like growth factors and colon cancer: A review of the evidence [J].
Giovannucci, E .
JOURNAL OF NUTRITION, 2001, 131 (11) :3109S-3120S
[34]  
GOMEZDESEGURA IA, 1995, REV ESP ENFERM DIG, V87, P288
[35]   Suppressors of cytokine signaling: Relevance to gastrointestinal function and disease [J].
Greenhalgh, CJ ;
Miller, ME ;
Hilton, DJ ;
Lund, PK .
GASTROENTEROLOGY, 2002, 123 (06) :2064-2081
[36]   Growth enhancement in suppressor of cytokine signaling 2 (SOCS-2)-deficient mice is dependent on signal transducer and activator of transcription 5b (STAT5b) [J].
Greenhalgh, CJ ;
Bertolino, P ;
Asa, SL ;
Metcalf, D ;
Corbin, JE ;
Adams, TE ;
Davey, HW ;
Nicola, NA ;
Hilton, DJ ;
Alexander, WS .
MOLECULAR ENDOCRINOLOGY, 2002, 16 (06) :1394-1406
[37]  
GUO YS, 1995, J AM COLL SURGEONS, V181, P145
[38]   COLORECTAL-CANCER IN ULCERATIVE-COLITIS - A COHORT STUDY OF PRIMARY REFERRALS FROM 3 CENTERS [J].
GYDE, SN ;
PRIOR, P ;
ALLAN, RN ;
STEVENS, A ;
JEWELL, DP ;
TRUELOVE, SC ;
LOFBERG, R ;
BROSTROM, O ;
HELLERS, G .
GUT, 1988, 29 (02) :206-217
[39]   Insulin resistance in the liver-specific IGF-1 gene-deleted mouse is abrogated by deletion of the acid-labile subunit of the IGF-binding protein-3 complex - Relative roles of growth hormone and IGF-1 in insulin resistance [J].
Haluzik, M ;
Yakar, S ;
Gavrilova, O ;
Setser, J ;
Boisclair, Y ;
LeRoith, D .
DIABETES, 2003, 52 (10) :2483-2489
[40]   CELLULAR-LOCALIZATION OF SOMATOMEDIN (INSULIN-LIKE GROWTH-FACTOR) MESSENGER-RNA IN THE HUMAN-FETUS [J].
HAN, VKM ;
DERCOLE, AJ ;
LUND, PK .
SCIENCE, 1987, 236 (4798) :193-197