Nutr Metab (Lond). 2026 Jun 27. doi: 10.1186/s12986-026-01158-5. Online ahead of print.
ABSTRACT
BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly prevalent and frequently associated with elevated liver enzymes, indicating hepatic injury. Although vitamin E has been investigated as a therapeutic antioxidant, its effects on liver enzyme levels remain inconsistent. This study aims to systematically review and quantitatively synthesize the evidence of the effects of vitamin E administration on liver enzymes in patients with MASLD.
METHODS: A systematic search of scientific databases was conducted up to September 2025 to identify relevant randomized clinical trials (RCTs). Data on alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and gamma-glutamyl transferase (GGT) were extracted. Pooled effect sizes were calculated as weighted mean differences (WMD) with 95% confidence intervals (CIs) using a random-effects model.
RESULTS: The pooled analysis of 16 RCTs (22 effect sizes) showed that vitamin E administration significantly reduced serum liver enzyme levels in patients with MASLD, including AST (WMD: -5.94 IU/L), ALT (WMD: -7.33 IU/L), ALP (WMD: -5.68 IU/L), and GGT (WMD: -5.54 IU/L), all with statistical significance (p ≤ 0.008). Subgroup analyses revealed that longer intervention durations and higher vitamin E doses were generally associated with greater improvements in liver enzyme levels, particularly AST and ALT. In contrast, Significant reductions in ALP were mainly observed in shorter trials and with lower vitamin E doses, especially at higher doses and among obese populations. Overall, benefits were consistent across BMI categories, though effects appeared more pronounced in obese individuals.
CONCLUSION: Vitamin E supplementation was associated with significant reductions in serum liver enzymes, suggesting improvement in hepatocellular injury and necroinflammatory activity in patients with MASLD. However, the available evidence is insufficient to determine its effects on fibrosis progression, metabolic burden, or long-term liver-related outcomes.
PMID:42374454 | DOI:10.1186/s12986-026-01158-5
