Published online May 15, 2024. doi: 10.4239/wjd.v15.i5.898
Peer-review started: January 4, 2024
First decision: January 17, 2024
Revised: January 29, 2024
Accepted: March 14, 2024
Article in press: March 14, 2024
Published online: May 15, 2024
Processing time: 126 Days and 20 Hours
Previous studies revealed that impaired metabolism of serum bile acid (BA) and unsaturated fatty acid (UFA) are associated with the onset and progression of type 2 diabetes mellitus (T2DM). However, the BA and UFA profiles and their alterations associated with the risk of developing Non-alcoholic fatty liver disease (NAFLD) remain unknown.
This study aims to delineate the differences in BA and UFA profiles between T2DM patients with and without NAFLD, seeking to elucidate the underlying pathogenic mechanisms of NAFLD in the context of T2DM.
To identify distinct metabolite biomarkers within BA and UFA profiles that are associated with NAFLD risk in individuals with T2DM.
A training model, consisting of 399 participants (113 healthy controls, 134 T2DM without NAFLD, and 152 T2DM with NAFLD), was established alongside an external validation model comprising 172 participants. NAFLD patients were stratified based on liver fibrosis scores. Fasting venous blood samples were collected from all subjects for the analysis of BA and UFA profiles, utilizing liquid chromatography coupled with tandem mass spectrometry.
Both T2DM and NAFLD groups exhibited lower levels of certain BAs compared to healthy controls. Certain UFAs demonstrated a positive correlation with NAFLD risk in T2DM. Levels of α-linolenic acid and γ-linolenic acid were associated with significant liver fibrosis in NAFLD, and validation confirmed their predictive power for NAFLD risk in T2DM patients.
Our findings reveal significant differences in serum BA and UFA profiles in T2DM patients with NAFLD compared to those without, suggesting a potential role in the pathogenesis of NAFLD.
To unravel the intricate interplay between NAFLD and T2DM, future research endeavors should encompass larger sample sizes and incorporate prospective studies or animal experiments, particularly focusing on the pathophysiological conditions influencing BA and UFA metabolism.
