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Decrease of liver glycogen content in golden hamsters infected with plerocercoids of Spirometra erinacei
Parasitology Research
|January 1, 1991
Summary
Spirometra erinacei infection in hamsters suppressed liver glycogen synthesis, not breakdown. This was linked to elevated glucagon levels, likely caused by parasite-induced hypoglycemia.
Area of Science:
- Parasitology
- Biochemistry
- Physiology
Background:
- Spirometra erinacei is a parasite that can infect various hosts.
- Liver glycogen plays a crucial role in glucose homeostasis.
- Understanding host-parasite interactions is vital for disease management.
Purpose of the Study:
- To investigate the effect of Spirometra erinacei infection on liver glycogen metabolism in golden hamsters.
- To determine the underlying mechanisms responsible for observed changes in glycogen content.
- To explore the role of insulin and glucagon in this host-parasite interaction.
Main Methods:
- Experimental infection of golden hamsters with Spirometra erinacei plerocercoids.
- Measurement of liver glycogen content.
- Assay of glycogen synthase a and glycogen phosphorylase a activity.
- Quantification of plasma immunoreactive insulin (IRI) and glucagon concentrations.
Main Results:
- Liver glycogen content was significantly decreased in infected hamsters.
- Glycogen synthase a activity was significantly reduced, while glycogen phosphorylase a activity remained unaffected.
- Plasma glucagon levels were significantly elevated in infected animals, whereas insulin levels showed no significant difference.
- Suppressed glycogenesis, not increased glycogenolysis, was identified as the cause of reduced glycogen levels.
Conclusions:
- Spirometra erinacei infection leads to suppressed liver glycogenesis in hamsters.
- Elevated glucagon levels, induced by parasite-induced hypoglycemia, are responsible for inhibiting glycogen synthase activity.
- This study elucidates a key metabolic disruption caused by Spirometra erinacei infection.