Introduction:
Galectin-3, a β-galactoside-binding protein, plays a crucial role in inflammation and insulin resistance in Type 2 Diabetes Mellitus (T2DM). This study investigated how Retatrutide, a novel GLP-1/GIP/glucagon receptor triple agonist, modulates the Galectin-3 pathway. Recent advances in multi-omics data analysis have highlighted the complexity of Galectin-3 signaling in Type 2 Diabetes Mellitus (T2DM). This bioinformatic study employed network analysis and pathway modeling to elucidate how Retatrutide, a novel triple receptor agonist, influences the Galectin-3 regulatory network.
Methodology:
We developed a computational framework integrating protein--protein interaction networks, pathway enrichment analysis, and dynamic modeling. Gene expression profiles were analyzed. This study incorporated regulatory network construction focusing on LGALS3 and associated genes, pathway topology analysis, and temporal expression pattern modeling. Key pathway components were mapped using directed graph theory and centrality metrics.
Results:
Network analysis identified five major regulatory hubs within the Galectin-3 pathway, with LGALS3 showing high betweenness centrality (0.85). Pathway enrichment revealed significant modulation of inflammatory cascades (p<0.001) and insulin signaling networks (p<0.01). Temporal expression modeling demonstrated biphasic regulation of LGALS3, with early suppression (-40%) followed by sustained down regulation. Graph theory analysis identified novel regulatory motifs linking GLP-1R activation to LGALS3 suppression through cAMP-dependent pathways.
Conclusion:
Our bioinformatic approach revealed previously uncharacterized regulatory mechanisms in Retatrutide's modulation of the Galectin-3 pathway. Network topology analysis suggests that Retatrutide's effects are mediated through coordinated regulation of multiple signaling nodes, rather than linear pathway suppression. These computational findings provide a systems-level understanding of Retatrutide's mechanism of action and identify potential therapeutic targets for experimental validation.