Enhanced growth of small bowel in transgenic mice expressing human insulin-like growth factor I.

Published

Journal Article

BACKGROUND & AIMS: Growth hormone and insulin-like growth factor I (IGF-I) stimulate small bowel growth. The aim of this study was to analyze whether IGF-I mediates enterotrophic actions of growth hormone. METHODS: IGF-I transgenic mice that overexpress an IGF-I transgene driven by the mouse metallothionein I promoter and are growth hormone deficient were compared with wild-type littermates. Growth of small bowel, abundance and localization of messenger RNAs for the IGF-I transgene, and insulin-like growth factor-binding protein 3 were assayed. RESULTS: Small bowel length and mass were greater in IGF-I transgenic mice than in wild-type mice. Villus height, crypt depth, and crypt cell mitoses were greater in jejunum of transgenics than wild-type mice, but jejunal disacharidase activities were not increased. The transgene was expressed strongly in villus epithelial cells. Insulin-like growth factor-binding protein 3 messenger RNA was localized in the lamina propria. Regional expression of both correlated with the increase in mucosal mass. CONCLUSIONS: Effects of IGF-I overexpression on intestinal length and mucosal mass were similar to effects of growth hormone overexpression observed previously. Excess of IGF-I increased crypt cell proliferation, whereas excess of growth hormone did not increase crypt cell proliferation. IGF-I excess stimulated differentiation of intestinal epithelial cells less effectively than growth hormone excess.

Full Text

Duke Authors

Cited Authors

  • Ohneda, K; Ulshen, MH; Fuller, CR; D'Ercole, AJ; Lund, PK

Published Date

  • February 1997

Published In

Volume / Issue

  • 112 / 2

Start / End Page

  • 444 - 454

PubMed ID

  • 9024298

Pubmed Central ID

  • 9024298

International Standard Serial Number (ISSN)

  • 0016-5085

Digital Object Identifier (DOI)

  • 10.1053/gast.1997.v112.pm9024298

Language

  • eng

Conference Location

  • United States