Published online Mar 15, 2024. doi: 10.4239/wjd.v15.i3.418
Peer-review started: October 28, 2023
First decision: December 23, 2023
Revised: January 5, 2024
Accepted: February 18, 2024
Article in press: February 18, 2024
Published online: March 15, 2024
Processing time: 138 Days and 17.3 Hours
Metabolic dysfunction-associated fatty liver disease (MAFLD) is now recognized as a prevalent global chronic liver disorder, standing as the primary contributor to end-stage liver disease and cardiovascular complications. This condition imposes a significant economic burden on public health. Previous research has elucidated the pivotal role of angiopoietin-like protein 8 (ANGPTL8) in the pathogenesis and progression of MAFLD, showcasing variations across different disease stages. Understanding ANGPTL8's involvement in MAFLD development informs early intervention strategies and aids in reducing mortality.
This study was motivated by the need for a convenient laboratory indicator facilitating the early identification of MAFLD and dynamic monitoring of its progression. Providing early intervention strategies for MAFLD patients is crucial to delay disease progression and reduce mortality.
The primary objective of this study was to conduct a comparative analysis of serum ANGPTL8 levels between individuals with and without MAFLD, investigating the predictive value of ANGPTL8 in relation to MAFLD development and progression.
In this cross-sectional study, 160 patients were enrolled, with 80 (50%) diagnosed with MAFLD. MAFLD patients were further categorized into hepatic fibrosis and non-hepatic fibrosis groups based on the fibrosis-4 index. Logistic regression analysis and receiver operating characteristic curves were employed to explore the impact and predictive ability of serum ANGPTL8.
Compared with the non-MAFLD group, serum ANGPTL8 levels and the triglyceride-glucose (TyG) index were significantly elevated in the MAFLD group, positively correlated with MAFLD. The combined ANGPTL8 and TyG index showed high predictive accuracy for MAFLD. Similarly, in the liver fibrosis group, both ANGPTL8 and the TyG index were significantly increased, positively correlated with liver fibrosis, with robust predictive accuracy for MAFLD-associated liver fibrosis.
Serum ANGPTL8 appears pivotal in the pathogenesis and progression of MAFLD, emerging as a potential biomarker for predicting both MAFLD and its associated hepatic fibrosis. The combined assessment of serum ANGPTL8 levels and the TyG index enhances predictive accuracy. Understanding the underlying mechanisms linking ANGPTL8 with MAFLD provides valuable insights for early diagnosis, risk stratification, and timely intervention, ultimately alleviating the burden of this disease.
Future studies should consider expanding sample sizes and incorporating liver biopsy and other methods to distinguish MAFLD-related liver fibrosis. Longitudinal studies are necessary to analyze serum ANGPTL8 changes at each MAFLD stage, confirming the relationship between serum ANGPTL8 and the occurrence and progression of MAFLD.