Insulinlike Growth Factor 1 (IGF-1) Reduces Gut Atrophy and Bacterial Translocation After Severe Burn Injury

K. Fon Huang, Dai H. Chung, David N. Herndon

Research output: Contribution to journalArticle

97 Scopus citations

Abstract

Bacterial translocation after severe burns is associated with gut mucosal atrophy and increased mucosal permeability. Insulinlike growth factor 1 (IGF-1) levels are low after trauma and do not respond to growth hormone treatment. Since IGF-1 receptors have been demonstrated in gut mucosa, we proposed that treatment with IGF-1 would reduce mucosal atrophy and bacterial translocation. Rats received 50% total body surface area full-thickness burn or sham burn. They were treated with a continuous, subcutaneous infusion of either IGF-1 (≈3 mg/kg per day) or placebo (0.01 mol of acetate) for up to 5 days after receiving the burn. The mesenteric lymph node and liver were cultured for gram-negative bacteria. The small intestinal mucosa was scraped, weighed, and analyzed for DNA and protein content. Treatment with IGF-1 improved body weight, spleen weight, and gut mucosal weight. It stimulated mucosal DNA and protein content and reduced the incidence of bacterial translocation to the mesenteric lymph node from 89% to 30%. Insulinlike growth factor may reduce gut barrier failure by decreasing mucosal atrophy and subsequent barrier failure. In addition to its general anabolic effects, recombinant human IGF-1 may improve gut mucosal function and reduce infectious morbidity in severely traumatized or septic patients by reducing gut atrophy and reducing bacterial translocation.

Original languageEnglish (US)
Pages (from-to)47-54
Number of pages8
JournalArchives of Surgery
Volume128
Issue number1
DOIs
StatePublished - Jan 1993
Externally publishedYes

ASJC Scopus subject areas

  • Surgery

Fingerprint Dive into the research topics of 'Insulinlike Growth Factor 1 (IGF-1) Reduces Gut Atrophy and Bacterial Translocation After Severe Burn Injury'. Together they form a unique fingerprint.

  • Cite this