Inflammatory Gene Expression, Insulin Resistance, and Circulating Markers Vary by Visceral Adiposity in Patients with Metabolic Dysfunction-Associated Steatotic Liver Disease.

BACKGROUND

Metabolic dysfunction-associated steatotic liver disease (MASLD) is driven by complex immune and inflammatory mechanisms. Visceral adiposity, a key contributor, worsens inflammation, immune dysregulation, and insulin resistance.

OBJECTIVE

This study examines correlations between inflammatory genes, insulin resistance markers, and inflammatory markers across visceral adiposity levels in patients with MASLD.

METHODS

This cross-sectional study included 102 patients with MASLD. Assessments included body mass index, visceral adiposity index (VAI), a body shape index (ABSI), inflammatory markers, gene expression from peripheral white blood cells, and serologic inflammatory proteins. We calculated insulin resistance markers, such as homeostasis model assessment-insulin resistance index (HOMA-IR), triglyceride/high-density lipoprotein cholesterol (TG/HDL-C) ratio, triglyceride-glucose (TyG) index, and neutrophil-to-HDL ratio (NHR). Pearson correlation coefficients evaluated parameter associations between low and high VAI and ABSI groups.

RESULTS

The higher VAI group presented with some elevated markers, such as HOMA-IR (5.21 ± 3.42 vs. 4.34 ± 4.62), TG/HDL-C (4.08 ± 1.97 vs. 2.20 ± 1.07), TyG (9.03 ± 0.48 vs. 8.70 ± 0.51), and NHR (1.86 ± 0.75 vs. 1.45 ± 0.64) compared with the low VAI group, indicating potentially greater insulin resistance and systemic inflammation. Monocyte chemoattractant protein-1 and interleukin-6 genes were strongly correlated in the low VAI group (R = 0.94, P < 0.001) but more weakly correlated in the high VAI group (R = 0.63, P < 0.001).

CONCLUSION

These findings highlight differential immune changes across visceral adiposity levels in MASLD, supporting the need for tailored interventions based on adiposity profiles.