Loading
Life sciences · Journal article
Hepatology Research · October 16, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
BACKGROUND: Lean metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized. Whether it represents a distinct entity or a phenotype within the MASLD spectrum remains unclear. We examined differences in risk factor contribution and metabolic trajectories. METHODS: In a longitudinal health checkup cohort (2017-2025), we included individuals without hepatic steatosis at baseline and excluded those with alcohol intake at or above the MetALD threshold. Incident MASLD was classified at diagnosis as Obese or Lean MASLD based on obesity status (BMI/WC). Baseline risk factors were evaluated using time-to-event and competing-risk models with interaction testing. Longitudinal metabolic changes were assessed using logistic regression, and repeated trajectories were examined using linear mixed-effects models. RESULTS: Among 13,624 participants, 1865 developed incident MASLD (Obese MASLD, n = 1469; Lean MASLD, n = 396). Male sex, baseline obesity, glycemic abnormality/diabetes, hypertension, hypertriglyceridemia, and higher baseline ALT were independently associated with incident MASLD. Interaction analyses showed a stronger contribution of male sex and weaker contributions of hypertension and low HDL-C in Lean MASLD. Longitudinal analyses showed Δtriglycerides and ΔALT were consistently associated with incident MASLD in both phenotypes, whereas ΔBMI showed a stronger association with Obese MASLD. CONCLUSIONS: Lean MASLD shared a broadly similar cardiometabolic risk structure with Obese MASLD, whereas the relative contribution of risk factors differed between phenotypes. Male sex showed a stronger association with Lean MASLD, whereas longitudinal changes in triglycerides and ALT were consistently associated with incident MASLD across both phenotypes. These findings provide exploratory evidence of phenotype-specific metabolic associations requiring validation before clinical application.