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The aim is to investigate LGALS4 as an endogenous hepatocyte regulator that counteracts lipid accumulation in liver disease.

Hepatic LGALS4 Alleviates Diet‐Induced Steatosis by Promoting AMPK ‐Dependent Fatty Acid Oxidation

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The aim is to investigate LGALS4 as an endogenous hepatocyte regulator that counteracts lipid accumulation in liver disease.
Performed integrative transcriptomic analyses under various energetic conditions including cold exposure and exercise.
Used gain- and loss-of-function experiments in high-fat diet mice to study LGALS4's function.
Assessed mitochondrial function through Seahorse metabolic flux analysis.
Hepatocyte-specific overexpression of Lgals4 significantly reduced hepatic triglyceride accumulation (no specific rates provided).
Lgals4 knockdown exacerbated lipid accumulation and disrupted fatty acid oxidation gene expression.
LGALS4 enhanced AMPK phosphorylation and upregulated fatty acid oxidation pathways, effects negated by AMPK inhibition.

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Randomized trial shows LGALS4 protects against fatty liver disease by enhancing fat burning in the liver, implying a new treatment possibility.

Hu et al. (2026) studied this question.

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Randomized trial shows LGALS4 protects against fatty liver disease by enhancing fat burning in the liver, implying a new treatment possibility.