Boron symbiotaxis: A trace element perspective on host-microbiome signaling and lipidomic coherence in obesity

Boron (B) is a biologically relevant trace element whose role in human physiology is still interpreted predominantly through dietary intake, systemic absorption, and measurable circulating levels. Although this absorption-centered framework has been useful, it may underestimate B-dependent functions within compartmentalized biological microenvironments, particularly at mucosal host-microbiome interfaces. In obesity, metabolic dysfunction is increasingly understood not merely as an energy imbalance, but as a disorder of host-microbiome integration characterized by gut microbial dysregulation, barrier dysfunction, low-grade inflammation, and membrane lipid remodeling, especially ceramide accumulation and altered microdomain organization that impair insulin signaling. Here, we propose a trace-element-centered framework that integrates dual-access B availability, distinguishing plasma-accessible B from microbiota-accessible B complexes, with the concept of B symbiotaxis, defined as B-dependent stabilization of microbial communication equilibria, including borate-complexed autoinducer-2 signaling. We hypothesize that reduced functional B availability in the gut may weaken microbial network coherence, destabilize short-chain fatty acid signaling, increase endotoxemic pressure, and thereby promote lipidomic incoherence characterized by ceramide enrichment, membrane rigidity, and impaired metabolic flexibility. This perspective extends the biological interpretation of B beyond a systemic micronutrient or metabolic cofactor toward a potential regulator of symbiotic information architecture linking microbiome organization to membrane-level metabolic regulation. We also discuss current evidential limitations and outline experimentally testable predictions and a translational roadmap spanning B speciation, microbial signaling assays, lipidomic profiling, and integrated biomarkers of metabolic resilience.