Molecular mechanisms of boron in animal nutrition: from cellular signalling to systemic metabolic regulation

Boron is essential for higher plants and biologically active in animals, although its essentiality in mammals remains unproven because no boron-dependent enzyme, cofactor, or consistent deficiency syndrome has been established. This review critically examines the biochemical, cellular, and physiological roles of boron in animal nutrition, emphasizing chemical speciation, dose dependence, and mechanistic uncertainty. As a weak Lewis acid, boron forms reversible complexes with cis-diol-containing biomolecules, potentially influencing membrane function, calcium homeostasis, redox regulation, and metabolic signaling without acting as a classical enzymatic cofactor. Inorganic boron compounds are generally well absorbed and predominantly excreted unchanged in urine, whereas the disposition and biological effects of organic boron complexes remain less characterized. Experimental evidence associates low, diet-relevant boron exposure with improved mineral utilization, skeletal integrity, antioxidant defenses, and metabolic and immune responses, although outcomes vary across species and experimental conditions. In several animal studies, 3–5 mg B/kg diet represents a low supplementation range, whereas 10–50 mg/kg and ≥100 mg/kg have been investigated as elevated and high exposures, respectively; these are not universal thresholds. Although boron participates in bacterial autoinducer-2 signaling, proposed microbiota-mediated benefits in animals remain largely hypothetical. Higher exposures may cause reproductive, developmental, and metabolic toxicity, suggesting a potentially biphasic dose–response relationship. Future research should establish species-specific exposure–response relationships, characterize biologically active boron forms, and validate causal mechanisms to support evidence-based nutritional recommendations.