Inflammatory Crosstalk Between Type 2 Diabetes and Sarcopenia: Insights from In Silico Evaluation

Sarcopenia and type 2 diabetes mellitus (T2DM) are chronic conditions that gradually affect the elderly, often coexisting and interacting in complex ways. Sarcopenia, which is characterized by the progressive loss of muscle mass and function, is frequently observed in individuals with T2DM. Although the clinical association is well known, the molecular mechanisms remain unclear. Gene expression datasets were retrieved from the Gene Expression Omnibus database. DEGs were identified using the limma package in R (R 4.4.0). Shared DEGs were subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Protein-protein interaction networks were constructed using the STRING database and were visualized with Cytoscape. Hub genes were identified via six topological algorithms in the CytoHubba plugin. Pearson's correlation analysis was conducted between hub genes and selected metabolic regulators. GO and KEGG enrichment analyses indicated that mitochondrial function, oxidative phosphorylation, and immune-inflammatory responses were significantly enriched. A PPI network revealed a mitochondrial hub of five key genes involved in energy metabolism, whose downregulation suggests mitochondrial dysfunction as a shared mechanism in sarcopenia and T2DM. Our results provide new insight into the molecular overlap between T2DM and sarcopenia, highlighting potential biomarkers and therapeutic targets for addressing both metabolic disruption and muscle decline.