FSTL3 partially mediates the association of increased nonalcoholic fatty liver disease fibrosis risk with acute myocardial infarction in patients with type 2 diabetes mellitus
Authors' conclusion
NAFLD fibrosis was closely associated with AMI in T2DM patients. FSTL3 expression was enriched in the liver of NAFLD patients with significant and advanced fibrosis, and serum FSTL3 partially mediated the association of increased liver fibrosis risk with AMI in T2DM patients.
Study context
- Population
- Patients with T2DM, with or without co-existent NAFLD
- Participants
- 1,424 patients
- Exposure
- T2DM with NAFLD vs T2DM without NAFLD; NAFLD fibrosis risk categories
- T2DMn = 429reference
- T2DM with NAFLDn = 995
- Outcome
- Association of NAFLD fibrosis risk with AMI and mediation by serum FSTL3
Methodological detailsmediation analysis, immunohistochemistry, Gene Expression Omnibus (GEO) database analysis
- Mediation analysis
- Immunohistochemistry
- GEO database analysis
Main finding
As reported in the abstract
- Increased NAFLD fibrosis risk was an independent risk factor for acute myocardial infarction (AMI) in T2DM with co-existent NAFLD
- Increased serum FSTL3 partially mediated the association of increased NAFLD fibrosis risk with AMI in T2DM with co-existent NAFLD
Observational data: associations, not effects.
Further findings
Liver FSTL3 expression
- GEO analysis and immunohistochemistry confirmed increased liver FSTL3 expression in NAFLD patients with fibrosis
- Immunohistochemistry in 60 NAFLD patients
Serum FSTL3
- Serum FSTL3 significantly increased in patients with high NAFLD fibrosis risk and AMI, and closely associated with NAFLD fibrosis and AMI severity
- 323 with serum samples (191 without AMI, 132 with AMI)
Original publication
FSTL3 partially mediates the association of increased nonalcoholic fatty liver disease fibrosis risk with acute myocardial infarction in patients with type 2 diabetes mellitus. Cardiovasc Diabetol. Published 30 October 2023. doi:10.
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