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Updated: Aug 2, 2026

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Published on: February 11, 2020
Zonal differences in ethanol-induced impairments in hepatic receptor binding
T M McCashland1, D J Tuma, M F Sorrell
1Liver Study Unit, VA Medical Center, Omaha, NE 68105.
Ethanol consumption impairs liver cell receptor function, particularly in the perivenule (PV) region. This study highlights selective damage to receptor-mediated endocytosis and recycling in the centrilobular liver area.
Area of Science:
- Hepatology
- Cell Biology
- Toxicology
Background:
- Ethanol consumption is known to cause liver damage.
- Receptor-mediated endocytosis is crucial for liver function.
- Previous studies indicated ethanol-induced defects in endocytosis.
Purpose of the Study:
- To compare ligand binding and receptor function in different liver zones (periportal and perivenule) after ethanol feeding.
- To investigate the regional selectivity of ethanol's effects on receptor-mediated endocytosis.
Main Methods:
- Isolated rat hepatocytes from periportal (Zone 1) and perivenule (Zone 3) regions were used.
- Binding assays were performed for asialoorosomucoid (ASOR), epidermal growth factor (EGF), and insulin.
- Receptor recycling efficiency was assessed in different liver regions.
Main Results:
- Ethanol feeding significantly decreased EGF binding in the perivenule region (40%) compared to controls.
- Both periportal and perivenule cells showed impaired ASOR binding after ethanol exposure, with greater impairment in the perivenule region (50-55%).
- Insulin binding was reduced by 20-25% in both regions. ASOR receptor recycling was more impaired in the perivenule region.
Conclusions:
- Ethanol selectively impairs receptor-mediated endocytosis and receptor recycling in the centrilobular (perivenule) region of the rat liver.
- These findings suggest a specific vulnerability of the perivenule region to ethanol-induced functional deficits.
- The study identifies a potential mechanism for liver dysfunction in chronic alcohol consumption.
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