Insulin-like growth factor-I (IGF-I) attenuates jejunal atrophy in association with increased expression of IGF-I binding protein-5 in parenterally fed mice

J Nutr. 2005 Nov;135(11):2553-9. doi: 10.1093/jn/135.11.2553.

Abstract

Total parenteral nutrition (TPN) induces dramatic mucosal hypoplasia in rat small intestine that is attenuated by insulin-like growth factor-I (IGF-I). Our aim was to determine the extent of TPN-induced intestinal atrophy and its response to infusion of IGF-I in mice. Male C57BL/6 mice (18-22 g) were maintained with TPN, TPN plus co-infusion of recombinant human IGF-I [2.5 mg/(kg . d)] or oral feeding for 5 d. Body weights did not differ among the groups although serum IGF-I was increased by 78% with IGF-I infusion. IGF-I prevented the significant 25% reduction in mass of the intact small intestine due to TPN compared with oral feeding. Greater TPN-induced atrophy was noted in duodenum and jejunum than ileum. Jejunal atrophy induced by TPN reflected significant decreases in muscularis mass and concentrations of protein and DNA; mucosal cellularity was not altered by TPN. TPN induced a significant decrease in jejunal muscularis width that was reversed by IGF-I with no differences in mucosal villus height and crypt depth. Local expression of IGF-I binding protein (IGFBP)-5 positively modulates the intestinotrophic effects of IGF-I. Jejunal atrophy due to TPN and growth due to IGF-I were directly associated with expression of IGFBP-5 mRNA. TPN decreased IGFBP-5 mRNA by 60% and IGF-I increased IGFBP-5 mRNA by 200% with no change in IGF-I mRNA compared with oral feeding. In summary, TPN induces significant 25% atrophy of the mouse small intestine that is attenuated by IGF-I in association with increased expression of IGFBP-5. Compared with rats, TPN-induced atrophy is less severe and occurs primarily in the jejunal muscularis layer in mice.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Body Weight
  • Gene Expression*
  • Insulin-Like Growth Factor Binding Protein 5 / blood
  • Insulin-Like Growth Factor Binding Protein 5 / genetics*
  • Insulin-Like Growth Factor Binding Protein 5 / physiology
  • Insulin-Like Growth Factor I / analysis
  • Insulin-Like Growth Factor I / genetics
  • Insulin-Like Growth Factor I / pharmacology*
  • Intestinal Mucosa / enzymology
  • Intestines / pathology
  • Jejunum / chemistry
  • Jejunum / pathology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Parenteral Nutrition, Total*
  • RNA, Messenger / analysis
  • Sucrase / metabolism

Substances

  • Insulin-Like Growth Factor Binding Protein 5
  • RNA, Messenger
  • Insulin-Like Growth Factor I
  • Sucrase