Preliminary evidence that non-fasting serum asprosin differs by sex but not by fibrosis stage in chronic hepatitis C
- 1Department of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology, Rheumatology, and Infectious Diseases, University Hospital Regensburg
Abstract
Background Asprosin is an adipokine increased in diabetes and fatty liver disease, two metabolic comorbidities frequently present in chronic hepatitis C virus (HCV) infection. Moreover, low serum asprosin levels were found in cirrhosis. However, its association with liver fibrosis stages in chronic HCV remains unclear. This study examined whether serum asprosin reflects liver disease severity in patients with chronic HCV. Methods Serum asprosin levels were measured by enzyme-linked immunosorbent assay before direct-acting antiviral (DAA) therapy, during treatment, and at sustained virological response 12 weeks after treatment (SVR12). Associations with liver fibrosis, cirrhosis, body mass index, sex, diabetes, hepatic steatosis, HCV viral load, genotype, and circulating lipids were analyzed. Results Higher serum asprosin in obese men, but not in obese women, was observed in chronic HCV. After exclusion of obese patients, women had higher serum asprosin levels than men. Serum asprosin did not differ in patients with or without diabetes and/or hepatic steatosis, irrespective of obesity status. It was not associated with liver fibrosis assessed by shear-wave elastography or fibrosis-4 score. Patients with ultrasound-defined cirrhosis had serum asprosin levels comparable to those without cirrhosis. Serum asprosin was also unrelated to liver function markers, the Model for End-Stage Liver Disease score, HCV viral load, or genotype. DAA therapy did not alter serum asprosin levels, which were 1.38 (0.32–4.61) ng/ml before therapy, 1.30 (0.16–2.27) ng/ml at 12 weeks of therapy, and 1.32 (0.40–3.75) ng/ml at SVR12. Females had modestly higher serum asprosin levels than males at therapy end and SVR12. Serum asprosin correlated positively with phosphatidylinositol and phosphatidylcholine before and after therapy. Conclusions Serum asprosin levels in chronic HCV show sex-specific differences. In contrast, it does not reflect metabolic comorbidities, liver fibrosis, cirrhosis, or virological features and remains stable during DAA therapy. Its positive relationship with circulating phospholipids before and after treatment suggests a role in lipid metabolism that merits further study.
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BibTeX
@article{peschel2026preliminary,
title = {{Preliminary evidence that non-fasting serum asprosin differs by sex but not by fibrosis stage in chronic hepatitis C}},
author = {Georg Peschel and Kilian Weigand and Martina Müller and Christa Buechler},
journal = {Egyptian Liver Journal},
year = {2026},
month = oct,
doi = {10.1186/s43066-026-00567-8},
url = {https://doi.org/10.1186/s43066-026-00567-8},
note = {CC BY},
}
RIS
TY - JOUR
TI - Preliminary evidence that non-fasting serum asprosin differs by sex but not by fibrosis stage in chronic hepatitis C
AU - Georg Peschel
AU - Kilian Weigand
AU - Martina Müller
AU - Christa Buechler
PY - 2026
DA - 2026/10/25
JO - Egyptian Liver Journal
DO - 10.1186/s43066-026-00567-8
UR - https://doi.org/10.1186/s43066-026-00567-8
AB - Background Asprosin is an adipokine increased in diabetes and fatty liver disease, two metabolic comorbidities frequently present in chronic hepatitis C virus (HCV) infection. Moreover, low serum asprosin levels were found in cirrhosis. However, its association with liver fibrosis stages in chronic HCV remains unclear. This study examined whether serum asprosin reflects liver disease severity in patients with chronic HCV. Methods Serum asprosin levels were measured by enzyme-linked immunosorbent assay before direct-acting antiviral (DAA) therapy, during treatment, and at sustained virological response 12 weeks after treatment (SVR12). Associations with liver fibrosis, cirrhosis, body mass index, sex, diabetes, hepatic steatosis, HCV viral load, genotype, and circulating lipids were analyzed. Results Higher serum asprosin in obese men, but not in obese women, was observed in chronic HCV. After exclusion of obese patients, women had higher serum asprosin levels than men. Serum asprosin did not differ in patients with or without diabetes and/or hepatic steatosis, irrespective of obesity status. It was not associated with liver fibrosis assessed by shear-wave elastography or fibrosis-4 score. Patients with ultrasound-defined cirrhosis had serum asprosin levels comparable to those without cirrhosis. Serum asprosin was also unrelated to liver function markers, the Model for End-Stage Liver Disease score, HCV viral load, or genotype. DAA therapy did not alter serum asprosin levels, which were 1.38 (0.32–4.61) ng/ml before therapy, 1.30 (0.16–2.27) ng/ml at 12 weeks of therapy, and 1.32 (0.40–3.75) ng/ml at SVR12. Females had modestly higher serum asprosin levels than males at therapy end and SVR12. Serum asprosin correlated positively with phosphatidylinositol and phosphatidylcholine before and after therapy. Conclusions Serum asprosin levels in chronic HCV show sex-specific differences. In contrast, it does not reflect metabolic comorbidities, liver fibrosis, cirrhosis, or virological features and remains stable during DAA therapy. Its positive relationship with circulating phospholipids before and after treatment suggests a role in lipid metabolism that merits further study.
SN - 2090-6226
ER -