Observational studyNutrients2025
Refining MASLD Phenotypes: Clinical, Metabolic, and Elastographic Differences Between Adipose Tissue Dysfunction and Obesity-Driven Disease.
Observational study in Nutrients, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Article
- Differential associations of traditional and shape-based adiposity indices with steatosis and fibrosis risk in metabolic dysfunction-associated steatotic liver disease.Journal of endocrinological investigation · 2026Article
- Immune Determinants of MASLD Progression: From Immunometabolic Reprogramming to Fibrotic Transformation.Biology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
objectivesMetabolic dysfunction-associated steatotic liver disease (MASLD) is a heterogeneous condition shaped by metabolic dysfunction, adipose tissue distribution, inflammatory activation, and body composition. Understanding how these factors interact across distinct clinical phenotypes is essential for improving diagnostic accuracy and risk stratification. This study aimed to compare metabolic, inflammatory, and elastographic profiles between MASLD subgroups defined by adipose tissue dysfunction (ATD) and obesity, and to identify pathways linking metabolic dysregulation to hepatic fibrosis.
methodsWe conducted a cross-sectional observational study including 178 adult participants evaluated clinically, biochemically, and by bioimpedance and shear wave elastography. Participants ranged in age from 19 to 82 years. Patients were stratified into a non-MASLD control group and two MASLD subgroups: MASLD with ATD (G1) and MASLD with obesity (G2). Anthropometric data, lipid profile, glycemic markers, cytokines (IL-6, IL-10, TNF-α), liver stiffness, and non-invasive fibrosis indices were compared across groups using standard statistical testing.
resultsPatients with MASLD showed higher liver stiffness, triglycerides, and IL-6/IL-10 levels than controls. Between MASLD phenotypes, the ATD group (G1) exhibited a more inflammatory and dysmetabolic profile, with significantly higher triglycerides, IL-6 levels, neutrophil counts, and creatinine, alongside trends suggesting early sarcopenic changes. In contrast, the obese phenotype (G2) demonstrated greater hepatic structural involvement, including higher liver stiffness and BMI, AST/ALT ratio and Diabetes (BARD) scores, despite more favorable inflammatory parameters. Several associations between liver stiffness, IL-6, and glycemic control approached but did not reach statistical significance.
conclusionsMASLD progression appears to follow two complementary but distinct mechanisms: an inflammatory, adipose dysfunction pathway dominated by IL-6 activation and early anabolic decline, and a metabolic-overload pathway driven by obesity. Phenotype-specific evaluation integrating inflammatory markers, metabolic indices, and elastographic parameters may improve risk stratification and inform personalized therapeutic strategies.
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