Metabolic syndrome and related disorders · 2026
Inflammatory Gene Expression, Insulin Resistance, and Circulating Markers Vary by Visceral Adiposity in Patients with Metabolic Dysfunction-Associated Steatotic Liver Disease.
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Lin Yi-Hsuan, Ma Chia-Chen, Tsai Shin-Yu, Hong Shiao-Ya, Yang Ying-Ying, Su Chien-Wei, Shen Hsiao-Chin, Hou Ming-Chih
Аннотация
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.
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.