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Related Experiment Video

Updated: Jan 17, 2026

Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis
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α1-acid Glycoprotein mitigates MASLD progression by modulating liver and adipose tissue function.

Ayano Nishinoiri1, Kai Tokumaru1, Gai Kanazawa2

  • 1Department of Clinical Pharmacy and Therapeutics, Graduate School of Pharmaceutical Sciences, Kumamoto University, Kumamoto 862-0973, Japan.

Endocrinology
|January 15, 2026
PubMed
Summary

Decreased alpha-1-acid glycoprotein (AGP) levels worsen metabolic dysfunction-associated steatotic liver disease (MASLD). Supplementing AGP shows therapeutic potential by protecting liver and adipose tissues, suggesting AGP

Keywords:
AGPMASLDadipose tissue inflammationfatty acid β-oxidationhepatokinemitochondria

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Area of Science:

  • Hepatology
  • Metabolic Diseases
  • Biochemistry

Background:

  • Hepatokine dysregulation is implicated in metabolic dysfunction-associated steatotic liver disease (MASLD).
  • Alpha-1-acid glycoprotein (AGP), a hepatokine, is investigated for its role in MASLD progression.

Purpose of the Study:

  • To investigate the role of AGP in MASLD progression.
  • To evaluate AGP's therapeutic potential for MASLD.

Main Methods:

  • Analysis of hepatic RNA-seq datasets from MASLD patients.
  • Utilized a high-fat diet (HFD)-induced mouse model of MASLD.
  • Employed AGP-knockout (AGP-KO) mice and exogenous human AGP (hAGP) administration.

Main Results:

  • Hepatic AGP gene expression decreased with MASLD progression.
  • AGP-KO mice on HFD showed exacerbated steatosis, obesity, inflammation, and impaired glucose tolerance.
  • hAGP protected against lipotoxicity and attenuated MASLD progression in mice by reducing mitochondrial dysfunction and adipose tissue inflammation.

Conclusions:

  • Reduced endogenous AGP levels may drive MASLD progression.
  • AGP demonstrates potential as a novel therapeutic agent for MASLD, targeting both liver and adipose tissue.