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Molecular Mechanisms Involved in MAFLD in Cholecystectomized Patients: A Cohort Study
Shreya C Pal1, Stephany M Castillo-Castañeda2,3, Luis E Díaz-Orozco1
1Faculty of Medicine, National Autonomous University of Mexico, Tlalpan, Mexico City 04510, Mexico.
Abstract:
Gallstone disease and metabolic dysfunction-associated fatty liver disease (MAFLD) share numerous common risk factors and progression determinants in that they both manifest as organ-specific consequences of metabolic dysfunction. Nevertheless, the precise molecular mechanisms underlying fibrosis development in cholecystectomized MAFLD patients remain inadequately defined. This study aimed to investigate the involvement of farnesoid X receptor 1 (FXR1) and fibroblast growth factor receptor 4 (FGFR4) in the progression of fibrosis in cholecystectomized MAFLD patients. A meticulously characterized cohort of 12 patients diagnosed with MAFLD, who had undergone liver biopsies during programmed cholecystectomies, participated in this study. All enrolled patients underwent a follow-up regimen at 1, 3, and 6 months post-cholecystectomy, during which metabolic biochemical markers were assessed, along with elastography, which served as indirect indicators of fibrosis. Additionally, the hepatic expression levels of FGFR4 and FXR1 were quantified using quantitative polymerase chain reaction (qPCR). Our findings revealed a robust correlation between hepatic FGFR4 expression and various histological features, including the steatosis degree (r = 0.779, p = 0.023), ballooning degeneration (r = 0.764, p = 0.027), interphase inflammation (r = 0.756, p = 0.030), and steatosis activity score (SAS) (r = 0.779, p = 0.023). Conversely, hepatic FXR1 expression did not exhibit any significant correlations with these histological features. In conclusion, our study highlights a substantial correlation between FGFR4 expression and histological liver damage, emphasizing its potential role in lipid and glucose metabolism. These findings suggest that FGFR4 may play a crucial role in the progression of fibrosis in cholecystectomized MAFLD patients. Further research is warranted to elucidate the exact mechanisms through which FGFR4 influences metabolic dysfunction and fibrosis in this patient population.
Insights
Fibroblast growth factor receptor 4 (FGFR4) expression correlates with liver damage in patients with metabolic dysfunction-associated fatty liver disease (MAFLD) after gallbladder removal. FXR1 did not show significant links to fibrosis progression.
Area of Science:
- Hepatology
- Metabolic Diseases
- Molecular Biology
Background:
- Gallstone disease and MAFLD share metabolic risk factors.
- Fibrosis mechanisms in MAFLD patients post-cholecystectomy are unclear.
- FXR1 and FGFR4 roles in MAFLD fibrosis require investigation.
Purpose of the Study:
- To investigate the involvement of FXR1 and FGFR4 in fibrosis progression.
- To assess the correlation between FGFR4/FXR1 expression and liver histology in MAFLD patients post-cholecystectomy.
Main Methods:
- Studied 12 MAFLD patients who underwent cholecystectomy and liver biopsy.
- Assessed metabolic markers and elastography at 1, 3, and 6 months post-surgery.
- Quantified hepatic FGFR4 and FXR1 expression using qPCR.
Main Results:
- Hepatic FGFR4 expression strongly correlated with steatosis degree (r=0.779, p=0.023), ballooning (r=0.764, p=0.027), inflammation (r=0.756, p=0.030), and SAS (r=0.779, p=0.023).
- Hepatic FXR1 expression showed no significant correlation with histological features.
- FGFR4 expression is linked to histological liver damage in this cohort.
Conclusions:
- FGFR4 expression is substantially correlated with histological liver damage in MAFLD patients post-cholecystectomy.
- FGFR4 may play a role in lipid and glucose metabolism and fibrosis progression in MAFLD.
- Further research is needed to clarify FGFR4's precise mechanisms in MAFLD fibrosis.
