Increased insulin-like growth factor and platelet-derived growth factor system in the pyloric muscle in infantile

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Updated: Oct 23, 2026

A Mouse Model of Intestinal Partial Obstruction
07:33

A Mouse Model of Intestinal Partial Obstruction

Published on: March 5, 2018

K Ohshiro1, P Puri

  • 1Children's Research Centre, Our Lady's Hospital for Sick Children, Dublin, Ireland.

Journal of Pediatric Surgery
|March 14, 1998
PubMed

Insights

Infantile hypertrophic pyloric stenosis (IHPS) shows increased insulin-like growth factor (IGF) and platelet-derived growth factor (PDGF) in pyloric muscle. These growth factors may contribute to the muscle thickening seen in IHPS.

Area of Science:

  • Gastroenterology
  • Developmental Biology
  • Cell Biology

Background:

  • Infantile hypertrophic pyloric stenosis (IHPS) involves pyloric muscle hypertrophy with unknown etiology.
  • Smooth muscle cell (SMC) growth is influenced by growth factors like IGF and PDGF.
  • IGF and PDGF signaling pathways, mediated by their receptors, are crucial for SMC proliferation.

Purpose of the Study:

  • To investigate the role of insulin-like growth factor (IGF) and platelet-derived growth factor (PDGF) systems in infantile hypertrophic pyloric stenosis (IHPS).
  • To compare the expression of IGF, PDGF, and their receptors in pyloric muscle tissue from IHPS patients and controls.

Main Methods:

  • Muscle biopsy specimens were collected from IHPS patients and age-matched controls.
  • Immunohistochemistry was used to detect IGF-I, IGF-I receptor alpha (IGF-IR alpha), IGF-IR beta, PDGF-BB, and PDGF receptor (PDGF-R).

Main Results:

  • IHPS tissues exhibited significantly elevated levels of IGF-I, IGF-IR alpha, IGF-IR beta, and PDGF-R in the circular muscle layer.
  • A lesser increase in these factors was observed in the longitudinal muscle layer of IHPS patients.

Conclusions:

  • Upregulation of local IGF and PDGF systems is implicated in the development of pyloric muscle hypertrophy in IHPS.
  • These findings suggest a potential molecular mechanism contributing to the pathophysiology of IHPS.
Abstract

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