25vzmnrw72 10.3205/25vzmnrw72 urn:nbn:de:0183-25vzmnrw724 Meeting Abstract Brisbois Brisbois Malvina M

Klinik für Gastroenterologie und Hepatologie, Universitätsklinikum des Saarlandes, Homburg, Deutschland

author Lambert Lambert Irina I

Klinik für Gastroenterologie und Hepatologie, Universitätsklinikum des Saarlandes, Homburg, Deutschland

author Karatayli Karatayli Senem S

Klinik für Gastroenterologie und Hepatologie, Universitätsklinikum des Saarlandes, Homburg, Deutschland

author Weber Weber Susanne N. SN

Klinik für Gastroenterologie und Hepatologie, Universitätsklinikum des Saarlandes, Homburg, Deutschland

author Krawczyk Krawczyk Marcin M

Klinik für Gastroenterologie, Hepatologie und Transplantationsmedizin, Essen, Deutschland

author German Medical Science GMS Publishing House

Düsseldorf

610 20250530 engl This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). M0616 72 Niederrheinisch-Westfälische Gesellschaft für Chirurgie Gesellschaft für Gastroenterologie in Nordrhein-Westfalen e.V. 191. Jahrestagung der Niederrheinisch-Westfälischen Gesellschaft für Chirurgie, 33. Jahrestagung der Gesellschaft für Gastroenterologie Viszeralmedizin NRW 2025 Gastroenterologie Essen 20250612 20250613 72 TextBackground: Type II diabetes (DMII) and metabolic dysfunction-associated steatotic liver disease (MASLD) are frequent conditions. The MTARC1 p.A165T variant has been identified as a protective factor against MASLD. This study evaluates the role of MTARC1 p.A165T as a genetic modulator of MASLD in DMII patients, alongside six additional MASLD-associated variants.Patients and Methods: A total of 124 DMII patients were prospectively enrolled. Liver steatosis and fibrosis were assessed using the controlled attenuation parameter (CAP) and liver stiffness measurement (LSM), respectively. Genetic variants, namely MTARC1 p.A165T, HSD17B13, PSD3, MBOAT7, PNPLA3, TM6SF2, and SERPINA1, were genotyped using TaqMan assays. Serum oxidative stress markers were evaluated in 40 patients with different MTARC1 genotypes using ELISA and colorimetric assays.Results: The median LSM was 6.6 kPa (range: 2–75 kPa), and the median CAP was 294 dB/m (range: 100–400 dB/m). MASLD was present in 52.4% of patients, and LSM > 15 kPa indicating cirrhosis was observed in 14.5% individuals. CAP showed significant correlations with BMI (p<0.01), HbA1c (p=0.02), triglycerides, LDL, and total cholesterol (p<0.05). LSM was significantly associated with bilirubin (p=0.01), alkaline phosphatase, and GGT (both p<0.01). The carriers of the MTARC1 p.A165T polymorphism exhibited an 11% reduction in maximal CAP and a 71% reduction in maximal LSM compared to non-carriers, along with higher serum TrxR2 levels (p=0.01). Variants in TM6SF2, MBOAT7, and PSD3 significantly influenced serum bilirubin, GOT, GGT, and GPT levels (all p<0.05).Conclusions: The prevalence of MASLD in this cohort aligns with previous findings in DMII populations. Genetic variants influence liver function markers in the setting of DMII, with MTARC1 modulating both steatosis and fibrosis. The association of MTARC1 genotypes with oxidative stress supports its protective role in liver disease. 0 0 0 0