Carbohydrate polymersSep 3, 2026

How Cichorium glandulosum polysaccharides may protect against muscle loss and obesity by triggering cell cleanup through the butyrate-GPR43-AMPK pathway

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Sep 4, 2026

Abstract

CGP-A, a novel branched fructan with a molecular weight of 6.722 kDa, may improve multiple metabolic parameters in db/db mice.

CGP-A reduced insulin resistance, liver fat accumulation, muscle loss, and intestinal barrier dysfunction in a dose-dependent manner.
Significant improvements in grip strength indicate enhanced muscle quality associated with CGP-A treatment.
CGP-A altered the gut microbiota by increasing levels of Ligilactobacillus, Bacteroides, and Alistipes, while also elevating serum butyrate.
Butyrate may activate the GPR43-AMPK signaling pathway in the liver and skeletal muscle, contributing to metabolic improvements.
Hepatic AMPK activation led to enhanced fatty acid oxidation, while muscular AMPK promoted mitochondrial function restoration and reduced protein degradation.
The beneficial effects of CGP-A were diminished following antibiotic treatment, highlighting the gut microbiota's role in mediating these outcomes.

Simplified

Sarcopenic obesity (SO) is a major complication of type 2 diabetes with limited therapeutic options. This study characterized CGP-A, a novel branched fructan (6.722 kDa) from Cichorium glandulosum. Its backbone consists of →1)-β-D-Fruf-(2→ and →6)-α-D-Glcp-(1→ residues, interspersed with →1,6)-β-D-Fruf-(2→ branching points. The side chains consist of terminal β-D-Fruf-(2→ units attached to the C-6 position of the fructofuranosyl residues in the backbone. In db/db mice, CGP-A dose-dependently ameliorated insulin resistance, hepatic steatosis, muscle loss and intestinal barrier dysfunction. Importantly, CGP-A significantly improved grip strength, reflecting an enhancement in muscle quality. Integrated multi-omics analysis combining metagenomics, multi-organ proteomics, and metabolomics revealed that CGP-A altered the gut microbiota, specifically enriching Ligilactobacillus, Bacteroides and Alistipes, while elevating serum butyrate. These findings suggest that butyrate may activate the GPR43-AMPK signaling pathway in both liver and skeletal muscle. Hepatic AMPK activation upregulated PPARα to enhance fatty acid oxidation; concurrently, muscular AMPK stimulated PINK1/Parkin-mediated mitophagy, restoring mitochondrial function and attenuating protein degradation. Antibiotic depletion abolished these effects, establishing the microbiota as a crucial mediator. These findings elucidate the gut microbiota-butyrate-GPR43-AMPK pathway through which CGP-A contributes to multi-organ metabolic improvements, offering a promising prebiotic strategy for managing SO.

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How Cichorium glandulosum polysaccharides may protect against muscle loss and obesity by triggering cell cleanup through the butyrate-GPR43-AMPK pathway

Abstract

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