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Updated: May 25, 2026

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen
Published on: November 27, 2019
Lipopolysaccharide binding protein is down-regulated during acute liver failure
Grace L Su1, Robert J Fontana, Kartik Jinjuvadia
1Veterans Administration Ann Arbor Healthcare Systems, Ann Arbor, MI, USA. gsu@umich.edu
Lipopolysaccharide binding protein (LBP) levels decrease in acute liver injury and failure, particularly after acetaminophen overdose. This finding may aid in developing new diagnostic and therapeutic strategies for liver failure patients.
Area of Science:
- Hepatology
- Immunology
- Biochemistry
Background:
- Lipopolysaccharide binding protein (LBP) modulates acetaminophen-induced (APAP) acute liver injury.
- LBP's biological activity is concentration-dependent, but its levels in acute liver failure remain understudied.
Purpose of the Study:
- To investigate serum and hepatic LBP levels in APAP-induced acute liver injury in mice.
- To assess serum LBP levels in patients with acute liver failure from various causes.
Main Methods:
- Measured serum and hepatic LBP in a mouse model of APAP-induced acute liver injury.
- Quantified serum LBP in patients with acute liver failure (APAP and non-APAP causes) and healthy controls.
Main Results:
- Serum and hepatic LBP levels were significantly decreased in mice 24 hours after APAP administration compared to controls.
- Similar reductions in LBP were observed in a carbon tetrachloride-induced liver injury mouse model.
- Patients with acute liver failure exhibited lower admission LBP levels compared to healthy controls, irrespective of the cause.
Conclusions:
- Serum and hepatic LBP levels significantly decrease early in severe acute liver injury/failure, including that caused by acetaminophen.
- This reduction in LBP is specific to acute liver failure and holds potential for future diagnostic and therapeutic applications.
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