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Gluconeogenesis in lethally X-irradiated rats
Summary
X-ray irradiation in rats increases glucose and glycogen in the liver by enhancing gluconeogenesis. Key enzyme activities, like phosphoenolpyruvate carboxykinase, rise post-irradiation, leading to glycogen accumulation.
Area of Science:
- Biochemistry
- Physiology
- Radiation Biology
Background:
- Radiation exposure significantly impacts metabolic processes.
- Understanding post-irradiation metabolic shifts is crucial for managing radiation injury.
Purpose of the Study:
- To investigate the effects of lethal X-ray doses on glucose and glycogen metabolism in rats.
- To examine the role of gluconeogenic enzymes in radiation-induced metabolic changes.
Main Methods:
- In vivo incorporation of U-14C-alanine into blood glucose and liver glycogen was measured.
- Activities of key gluconeogenic enzymes (phosphoenolpyruvate carboxykinase, glucose-6-phosphatase, fructose-1,6-diphosphatase) were analyzed in rat liver.
Main Results:
- Irradiation led to increased 14C-alanine incorporation into blood glucose and liver glycogen.
- Elevated phosphoenolpyruvate carboxykinase and glycogenic activity were observed from 6 to 48 hours post-irradiation, correlating with glycogen accumulation.
- Glucose-6-phosphatase activity decreased, showing a negative correlation with liver glycogen levels.
Conclusions:
- Glycogen accumulation in the liver and elevated blood glucose levels in X-irradiated rats are primarily due to enhanced gluconeogenesis.
- Specific gluconeogenic enzyme alterations are key mechanisms underlying metabolic dysregulation after lethal X-ray exposure.