Fucoidan P Alleviates Sarcopenic Obesity by Regulating Muscle Protein and Energy Metabolism

Area of Science:

• Biochemistry
• Molecular Biology
• Pharmacology

Background:

• Sarcopenic obesity (SO) is characterized by excess fat and muscle loss, with no current drug treatments.
• Akt and AMPK signaling pathways are crucial for muscle health and energy balance.
• Natural compounds modulating these pathways present a potential therapeutic avenue for SO.

Purpose of the Study:

• To investigate the effects of Fucoidan P on sarcopenic obesity (SO).
• To elucidate the molecular mechanisms underlying Fucoidan P's action on SO.
• To assess the translational relevance of Fucoidan P using clinical data.

Main Methods:

• Administered Fucoidan P to a high-fat diet-induced SO model.
• Analyzed changes in body weight, fat mass, muscle mass, and grip strength.
• Investigated molecular pathways including Akt, AMPK, mTOR, FOXO3a, SIRT1, PGC-1α, and NF-κB.
• Examined differentially expressed genes (PDE5A, PTGS1) in clinical datasets.

Main Results:

• Fucoidan P reduced body weight, fat mass, and size, while increasing muscle mass, grip strength, and muscle fiber size.
• It promoted muscle protein synthesis via Akt/mTOR/FOXO3a and enhanced energy metabolism via AMPK/SIRT1/PGC-1α.
• Fucoidan P downregulated inflammation-related genes (PDE5A, PTGS1) and inhibited pro-inflammatory cytokines by suppressing NF-κB.

Conclusions:

• Fucoidan P alleviates SO by regulating muscle homeostasis, energy metabolism, and inflammation.
• It acts through interconnected Akt, AMPK/PGC-1α, and NF-κB signaling pathways.
• Fucoidan P shows potential as a multi-target therapeutic agent for sarcopenic obesity.