Key result
MASLD was associated with ~7% lower HDL cholesterol (43 vs 46 mg/dL, P=0.004) and a shift from large HDL2b to small HDL3 particles (P<0.05) despite similar plasma triglycerides.
Cross-Sectional (n=79)
No
In males with abdominal obesity, MASLD is associated with lower HDL-cholesterol and a shift toward smaller HDL3 particles even in the absence of elevated plasma triglycerides and after adjusting for age and insulin resistance.
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MASLD-associated HDL remodeling should not yet guide therapy; leaves open independent cardiovascular risk prediction beyond triglycerides.
Background The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) is rising together with obesity. MASLD is often associated with elevated triglyceride concentrations, and hypertriglyceridemia is in turn linked to lower high-density lipoprotein (HDL) cholesterol levels. Little is known about the relationship between MASLD and HDL subclass distribution and particle composition, which reflect HDL’s function and maturation state. In this study, we characterized differences in HDL subclasses in healthy males with and without MASLD who had similar body mass index (BMI) and total body fat. Method The study included 79 males—44 with MASLD and 35 without (non-MASLD)—aged 30–70 years, with abdominal obesity and BMI between 28 and 45 kg/m2. HDL subclass distribution and composition was assessed with proton nuclear magnetic resonance spectroscopy. Lipoprotein characteristics were compared between groups using unadjusted statistical models and after adjusting for age and the homeostasis model assessment for insulin resistance (HOMA-IR) score. Results The MASLD group had ~ 8% lower HDL cholesterol concentration compared to the non-MASLD group (P = 0.004), but similar total plasma triglyceride levels (P = 0.24). There was a pronounced shift in the distribution of HDL particles away from larger HDL2b and towards smaller HDL3 particles in individuals with MASLD (P < 0.01). All lipid components of HDL2b particles, except triglyceride, were lower in MASLD, thus individual HDL2b particles (lipid ratios relative to apolipoprotein A1) were relatively enriched in triglyceride (68%). After adjusting for age and HOMA-IR, the shift in HDL subclass distribution remained significant, while differences in absolute and relative concentrations of HDL2b lipids became non-significant. Conclusion MASLD is associated with distinct alterations in HDL subclass distribution, and likely HDL metabolism, independently of hypertriglyceridemia. Further studies are needed to understand the mechanism behind these observations.
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Kobayashi et al. (2026) conducted a cross-sectional in Metabolic dysfunction-associated steatotic liver disease (MASLD) and abdominal obesity (n=79). Metabolic dysfunction-associated steatotic liver disease (MASLD, intrahepatic triglyceride >=5.6%) vs. Non-MASLD (intrahepatic triglyceride <5.6%) was evaluated on HDL cholesterol concentration (mg/dL) (MD -3 mg/dL (~7% lower), p=0.004). MASLD was associated with ~7% lower HDL cholesterol (43 vs 46 mg/dL, P=0.004) and a shift from large HDL2b to small HDL3 particles (P<0.05) despite similar plasma triglycerides.
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