Insights into Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis: The Role of Fibrinogen and Pepsinogen
Related Experiment Video
Updated: May 12, 2026

Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
Zahra Eslami1,2, Alireza Norouzi3,4,5
1Department of Clinical Biochemistry, Golestan University of Medical Sciences, Golestan, Iran.
Background:
Fibrinogen is a multifunctional protein that contributes to inflammatory processes. Elevated levels of fibrinogen have been associated with increased liver fibrosis and disease severity of non-alcoholic steatohepatitis (NASH). Fibrinogen appears to interact with other factors implicated in NASH pathophysiology, such as activation of immune cells to induce pro-inflammatory cytokines and cellular signaling pathways. Additionally, fibrinogen-mediated pathways may disrupt normal tissue repair processes. Pepsinogen, the inactive precursor of pepsin and a specific functional enzyme in the gastric mucosa, is a serological marker with subtypes closely related to different gastrointestinal diseases. Changes in pepsinogen levels in liver disease are not entirely understood and likely relate to many factors, including inflammation, altered gastrin levels, and Helicobacter pylori infection. The clinical implications of altered pepsinogen levels in liver disease are still under investigation, but they may have relevance in the diagnosis and monitoring of liver disease.
Methods:
Databases searched included PubMed, Google Scholar, and Scopus from 2005 to 2024, and the following keywords were used: fibrinogen, pepsinogen, non-alcoholic steatohepatitis, NASH, non-alcoholic fatty liver disease, NAFLD, and fibrosis.
Results:
As a potential biomarker for NASH, measuring fibrinogen levels could offer valuable insights into disease diagnosis and progression monitoring. On the other hand, pepsinogen is involved in gut health and liver function, contributing to liver inflammation and fibrosis through mechanisms like the gut-liver axis and signaling pathways.
Conclusion:
Overall, both fibrinogen and pepsinogen appear to have a more significant negative impact on liver health and the progression of NAFLD than beneficial effects. Integrating assessments of fibrinogen and pepsinogen into clinical practice could facilitate earlier intervention strategies aimed at slowing disease progression.
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