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Related Experiment Videos

Progressive decrease in tissue glycogen content in rats with long-term cholestasis

L Krahenbuhl1, C Talos, J Reichen

  • 1Department of Visceral and Transplantation Surgery, University Hospital, Zurich, Switzerland.

Hepatology (Baltimore, Md.)
|October 1, 1996
PubMed
Summary
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Bile duct ligation in rats progressively depleted liver and skeletal muscle glycogen. Reduced glycogen synthesis, indicated by lower enzyme activities, is the primary cause of this glycogen depletion.

Area of Science:

  • Biochemistry
  • Physiology
  • Hepatology

Background:

  • Bile duct ligation (BDL) is a model for cholestatic liver disease.
  • Glycogen metabolism is crucial for maintaining energy homeostasis in the liver and muscles.
  • The impact of BDL on glycogen metabolism requires further elucidation.

Purpose of the Study:

  • To investigate the effects of bile duct ligation (BDL) on liver and skeletal muscle glycogen metabolism in rats.
  • To determine the time-dependent changes in glycogen content and key metabolic enzymes.
  • To explore the relationship between glycogen metabolism and plasma glucagon levels.

Main Methods:

  • Rats underwent bile duct ligation (BDL) or sham operation.
  • Glycogen content and enzyme activities (glycogen synthase, glycogen phosphorylase) were measured in liver and skeletal muscle at 1 and 4 weeks post-surgery.

Related Experiment Videos

  • Morphometric analysis was used for liver glycogen quantification; plasma glucagon was measured.

    • Main Results:

    • BDL rats showed a progressive decrease in hepatic glycogen content at 1 and 4 weeks.
    • Activities and active fractions of hepatic glycogen synthase and phosphorylase were reduced in BDL rats.
    • Skeletal muscle glycogen content decreased significantly by 4 weeks post-BDL; plasma glucagon increased.

    Conclusions:

    • Bile duct ligation leads to significant, time-dependent reductions in hepatic and skeletal muscle glycogen.
    • Decreased glycogen synthesis, due to reduced glycogen synthase and phosphorylase activity, is the main mechanism for hepatic glycogen depletion.
    • Elevated plasma glucagon in BDL rats may contribute to altered glycogen metabolism.