Cellular and molecular pathways linking obesity to skeletal muscle dysfunction

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Obesity is increasingly recognized as a condition that directly impairs skeletal muscle structure, metabolism, and endocrine function through complex molecular and cellular mechanisms extending beyond the classical concept of sarcopenic obesity. This narrative review aimed to synthesize current evidence regarding the intracellular signaling pathways, metabolic alterations, and endocrine interactions involved in obesity-induced skeletal muscle dysfunction independent of overt sarcopenia. Relevant literature from experimental, clinical, and review studies was identified through searches of PubMed, Scopus, and Web of Science databases, focusing on obesity-associated alterations in skeletal muscle metabolism, ectopic lipid accumulation, inflammatory signaling, mitochondrial dysfunction, and adipose-muscle crosstalk. Current evidence indicates that obesity per se promotes skeletal muscle dysfunction through ectopic lipid deposition, lipotoxicity, mitochondrial impairment, and chronic low-grade inflammation mediated by dysregulated intracellular signaling pathways. Altered adipomyokine signaling, including interleukin-6 and tumor necrosis factor-α, further contributes to impaired insulin signaling, reduced metabolic flexibility, oxidative stress, and compromised muscle integrity. These molecular and cellular alterations reinforce skeletal muscle as both a target and an active regulat

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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