Related Experiment Video

Updated: Jan 16, 2026

Precise Visualization of Insulin Receptors A and B in Murine Brain with an RNA In Situ Hybridization Assay
08:34

Precise Visualization of Insulin Receptors A and B in Murine Brain with an RNA In Situ Hybridization Assay

Published on: July 15, 2025

656

Downregulation of insulin receptor isoform A in the forebrain of fetal growth-restricted rats

Yutaro Tomobe1, Seiichi Tomotaki2, Yukinori Yoshimura1

  • 1Department of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Pediatric Research
|September 27, 2025
PubMed

Insights

Fetal growth restriction reduces brain Insulin Receptor isoform A (IR-A) expression, particularly in the forebrain, potentially explaining poor neurodevelopmental outcomes in affected infants.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Endocrinology

Background:

  • Asymmetrical fetal growth restriction (FGR) is linked to poor neurodevelopmental outcomes in children.
  • Insulin receptor isoform A (IR-A) plays a crucial role in neurodevelopment.
  • The impact of FGR on brain IR-A expression remains unclear.

Purpose of the Study:

  • To investigate changes in brain IR-A expression in a neonatal rat model of FGR.
  • To explore the relationship between FGR, glucose metabolism, and IR-A expression in the brain.

Main Methods:

  • FGR was induced in rats via maternal caloric restriction (CR).
  • Brain and liver glucose uptake and gene expression (IR-A, GLUT) were compared between CR and control neonates.
  • RNA sequencing and immunohistochemistry were used to analyze gene expression and protein localization.

Main Results:

  • CR rats exhibited higher brain-to-liver weight and glucose uptake ratios.
  • Glucose transporter (GLUT) gene expression was maintained in the CR rat brain.
  • Overall brain IR-A expression was reduced in CR rats, with decreased expression in the forebrain but not the hindbrain.

Conclusions:

  • Reduced forebrain IR-A expression in FGR may contribute to impaired cognitive function and poor neurodevelopmental prognosis.
  • Regional differences in IR-A suggest an endocrinological mechanism regulating brain function during nutrient deficiency.
  • These findings highlight a potential mechanism underlying neurodevelopmental deficits in FGR.
Abstract

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