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Updated: Jun 19, 2026

The Murine Choline-Deficient, Ethionine-Supplemented (CDE) Diet Model of Chronic Liver Injury
Published on: October 21, 2017
CIRRHOSIS OF THE LIVER CAUSED BY EXCESS DIETARY CYSTINE
1Research Service, First Division, Welfare Hospital, Department of Hospitals, City of New York, and the Department of Medicine, College of Physicians and Surgeons, Columbia University, New York.
High dietary cystine levels in young rats caused severe liver damage, including necrosis and cirrhosis, and high mortality. Some liver regeneration was observed after dietary changes.
Area of Science:
- Biochemistry
- Toxicology
- Hepatology
Background:
- Dietary amino acids play crucial roles in metabolic processes.
- Excessive intake of certain nutrients can lead to adverse health effects.
- Understanding the impact of specific amino acids on liver function is vital.
Purpose of the Study:
- To investigate the toxicological effects of excess dietary cystine on the liver in young albino rats.
- To determine the dose-dependent relationship between cystine intake and observed pathologies.
- To assess the reversibility and regenerative capacity of liver damage.
Main Methods:
- Young albino rats were fed diets containing 5% or 10% cystine.
- Control groups were fed a standard diet.
- Histopathological examination of liver tissues was performed at various time points.
- Rats were also observed after returning to a standard diet to assess recovery.
Main Results:
- 10% dietary cystine induced acute portal hemorrhagic necrosis and high mortality within days.
- 5% dietary cystine led to fatty infiltration and subsequent necrosis, with cirrhosis developing in some rats.
- Livers showed signs of regeneration, including mitotic figures, after returning to a standard diet.
- Renal lesions were infrequent, observed in only one rat out of 30.
Conclusions:
- Excessive dietary cystine is hepatotoxic, causing dose-dependent liver injury.
- The liver exhibits regenerative potential following cessation of high cystine intake.
- Acute liver damage and fatty infiltration are primary consequences of high cystine consumption.
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