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Twenty-four hour fasting increases endotoxin lethality in the rat
A H Esahili1, P O Boija, O Ljungqvist
1Department of Surgery, University Hospital, Uppsala, Sweden.
The European Journal of Surgery = Acta Chirurgica
|February 1, 1991
Summary
Food deprivation significantly increases mortality from endotoxin (ET) in rats. Liver glycogen depletion exacerbates endotoxic shock, highlighting its protective role against ET lethality.
Area of Science:
- Physiology
- Toxicology
- Nutritional Science
Background:
- Endotoxemia, a condition caused by endotoxin (ET) exposure, can lead to severe physiological distress and mortality.
- Nutritional status is known to influence the body's response to various stressors, but its specific impact on endotoxemia requires further elucidation.
Purpose of the Study:
- To investigate the effect of 24-hour food deprivation on endotoxin lethality in Sprague-Dawley rats.
- To determine the relationship between endotoxin dose, nutritional status, and mortality.
- To explore the role of liver glycogen in the context of endotoxic shock.
Main Methods:
- Rats were subjected to 24-hour food deprivation or fed normally.
- Endotoxin was administered via intravenous infusion or intraperitoneal bolus at varying doses (LD10-LD80).
- Survival rates were monitored for seven days, and liver glycogen content and histopathological liver damage were assessed.
Main Results:
- Food-deprived rats exhibited significantly higher mortality rates (208-240% increase with IV ET, 87-200% with IP ET) compared to fed rats.
- A linear relationship was observed between endotoxin doses (LD10-LD80) and mortality.
- Endotoxin administration increased liver glycogen content in a dose-dependent manner in non-fasted rats, while fasted rats showed depleted glycogen levels.
- Histopathological liver damage and leucopenia were correlated with endotoxin dose and modified by nutritional status.
Conclusions:
- 24-hour food deprivation substantially increases mortality associated with endotoxin exposure in rats.
- Liver glycogen serves as a critical protective substrate resource during endotoxic shock.
- Nutritional status significantly modulates the severity of endotoxin-induced organ damage and lethality.