European journal of pharmacologyJul 14, 2026

Glucosamine may help improve alcoholic liver disease and slow liver aging by activating energy-regulating pathways

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Jul 15, 2026

Abstract

Glucosamine (GlcN) administration significantly reduced hepatic lipid accumulation and inflammation in mouse models of alcoholic liver disease (ALD).

GlcN was identified as a candidate for mitigating both ALD and liver aging.
In both acute and chronic mouse models, GlcN decreased pro-inflammatory cytokine expression and cellular senescence markers.
The treatment activated AMPK signaling, which may suppress the secretion of inflammatory factors associated with cellular aging.
GlcN improved lipid metabolism by regulating specific metabolic pathways involved in fat synthesis.
These findings suggest that GlcN may play a multifaceted role in addressing issues related to ALD and liver aging.

Simplified

Alcohol consumption is a major etiological factor for alcoholic liver disease (ALD) and accelerates liver aging, representing a progressive condition with limited therapeutic options. Recent evidence suggests that targeting hepatocellular senescence represents a promising therapeutic strategy, particularly through repurposing approved drugs capable of simultaneously ameliorating hepatic steatosis, inflammation, and liver aging. In this study, we screened reported anti-aging molecules and identified glucosamine (GlcN) as a candidate with the potential to mitigate both ALD and liver aging. In both acute and chronic mouse models of ALD, GlcN administration significantly reduced hepatic lipid accumulation, pro-inflammatory cytokine expression, and cellular senescence markers. Mechanistically, GlcN activated AMPK signaling, which subsequently suppressed the senescence-associated secretory phenotype (SASP) through modulation of the p38 MAPK pathway, and improved lipid metabolism by regulating the SREBP1/FAS and ACC pathways. These findings illustrate the multifaceted role of GlcN in ameliorating both cellular senescence and dysregulated lipid metabolism, thereby attenuating ALD progression. Our results support the repurposing of GlcN as a potential candidate for ALD and alcohol-associated liver aging.

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Glucosamine may help improve alcoholic liver disease and slow liver aging by activating energy-regulating pathways

Abstract

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