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Related Experiment Videos

Glycogen phosphorylase: developmental expression in rat liver

C A Bloch1, M A Ozbun, S A Khan

  • 1Department of Pediatrics, University of Colorado School of Medicine, Denver.

Biology of the Neonate
|January 1, 1993
PubMed
Summary

Fetal rats show increased hepatic glycogen phosphorylase mRNA and enzyme activity near term. Gene expression is regulated post-transcriptionally, likely via enhanced mRNA stability, ensuring adequate glucose supply for newborns.

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Area of Science:

  • Biochemistry
  • Developmental Biology
  • Molecular Endocrinology

Background:

  • Fetal vulnerability to hypoglycemia due to compromised transplacental substrate supply.
  • Hepatic glycogen phosphorylase is crucial for glucose homeostasis.

Purpose of the Study:

  • To investigate hepatic glycogen phosphorylase gene expression during late fetal and early neonatal development in rats.
  • To elucidate the regulatory mechanisms controlling glycogen phosphorylase expression in the developing liver.

Main Methods:

  • Quantification of hepatic phosphorylase enzyme activity (total and phosphorylase a).
  • Measurement of cellular phosphorylase mRNA concentrations using Northern blot or similar techniques.
  • Assessment of transcription rates via isolated liver nuclei assays at different gestational and postnatal ages.

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Main Results:

  • Hepatic phosphorylase enzyme activity and mRNA levels progressively increased from 19 days of gestation until term.
  • The rate of phosphorylase mRNA transcription was highest at 19 days of gestation and decreased significantly towards term.
  • A discrepancy between declining transcription rates and increasing mRNA levels suggests post-transcriptional regulation.

Conclusions:

  • Hepatic glycogen phosphorylase gene expression is primarily regulated post-transcriptionally in late fetal rat development.
  • Increased stability of phosphorylase mRNA towards term likely contributes to the observed rise in enzyme levels.
  • This regulatory mechanism ensures sufficient hepatic glycogenolytic capacity for neonatal glucose homeostasis.