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Refining MASLD Phenotypes: Clinical, Metabolic, and Elastographic Differences Between Adipose Tissue Dysfunction and
Tudor Cosma1, Lucretia Avram2, Valer Donca2
1Regional Institute of Gastroenterology and Hepatology "Prof. Dr. Octavian Fodor", Faculty of Medicine, "Iuliu Hatieganu" University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania.
Nutrients
|December 31, 2025
Summary
Metabolic dysfunction-associated steatotic liver disease (MASLD) progresses via distinct pathways: one driven by adipose dysfunction and inflammation, the other by obesity. Understanding these MASLD phenotypes is key for personalized treatment.
Area of Science:
- Hepatology and metabolic research, focusing on liver disease mechanisms.
- Investigating the interplay between metabolic health, inflammation, and liver structure.
- Exploring novel diagnostic and risk stratification approaches for liver conditions.
Background:
- Metabolic dysfunction-associated steatotic liver disease (MASLD) is complex, influenced by metabolic health, fat distribution, inflammation, and body composition.
- Distinct clinical phenotypes of MASLD exist, necessitating a deeper understanding for accurate diagnosis and risk assessment.
- Identifying the specific pathways linking metabolic issues to liver fibrosis is crucial.
Purpose of the Study:
- To compare metabolic, inflammatory, and elastographic profiles across MASLD subgroups defined by adipose tissue dysfunction (ATD) and obesity.
- To identify specific pathways connecting metabolic dysregulation to the development of hepatic fibrosis.
- To differentiate MASLD phenotypes for improved clinical management.
Main Methods:
- A cross-sectional observational study involving 178 adult participants.
- Stratification into non-MASLD controls, MASLD with ATD (G1), and MASLD with obesity (G2).
- Clinical, biochemical, bioimpedance, and shear wave elastography assessments, including cytokine analysis (IL-6, IL-10, TNF-α).
Main Results:
- MASLD patients exhibited higher liver stiffness, triglycerides, and IL-6/IL-10 levels compared to controls.
- The ATD group (G1) showed a more inflammatory and dysmetabolic profile with higher IL-6 and signs of sarcopenia.
- The obese group (G2) presented with greater hepatic structural involvement (higher liver stiffness, BMI, AST/ALT ratio) despite better inflammatory markers.
Conclusions:
- MASLD progression involves two distinct pathways: adipose dysfunction/inflammation (IL-6 driven) and metabolic overload/obesity.
- Phenotype-specific evaluation integrating inflammatory, metabolic, and elastographic data is vital.
- Personalized therapeutic strategies for MASLD can be informed by understanding these distinct pathways.
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