Effects of heat stress on physiological, endocrine, and reproductive functions in swine: review

초록

Heat stress (HS) induced by climate change significantly impacts the productive and reproductive performance of swine. Using temperature-humidity index for quantifying heat load as a framework, this review integrates HS effects across the endocrine and metabolic axis, the gut barrier microbiota, immune axis, and the reproductive axis. HS, within the context of hypothalamic, pituitary, adrenal (HPA) sympathetic–adrenomedullary activation and interactions among insulin, catecholamine, and cortisol crosstalk, results in relative hyperinsulinemia. This condition, via the mediation of pyruvate dehydrogenase kinase 4, inhibits pyruvate dehydrogenase and influences the lactate dehydrogenase/ hypoxia-inducible factor-1α (HIF-1α) axis, leading to a redistribution of substrate utilization towards glucose and constraining lipid mobilization. Short chain fatty acids (SCFA) depletion, β-diversity, and centered dysbiosis weaken HIF-1α-dependent mucosal barrier defenses within the gut immune axis. This, along with increased lipopolysaccharide translocation, hyperactivates TLR4/NF-κB signaling, the NLR family pyrin domain containing 3 inflammasome, and Th17/IL-17 pathways. Fecal microbiota transplantation evidence supports a causal relationship between dysbiosis and pathogenesis. Dysregulated crosstalk within the hypothalamic–pituitary–gonadal–HPA axis adversely affects both follicular and luteal function, as well as placental nutrient transport. Intrauterine HS can reprogram F1 offspring, resulting in lasting effects on metabolism, immunity, and reproductive capabilities. In conclusion, HS functions as a systems-level stressor that perturbs multiple physiological axes. Advancement in this field necessitates the development of standardized HS models, the application of multi-omics approaches and multigenerational follow-up studies, and the integration of environmental, nutritional, and management strategies. Shifts in beta diversity the gut microbiota and SCFA depletion emerged as core pathophysiologic mediators. These findings support for their potential use as early biomarkers and intervention targets, underscoring the need for targeted investigation.

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