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Updated: Aug 5, 2026

Prevention of Heat Stress Adverse Effects in Rats by Bacillus subtilis Strain
Published on: July 11, 2016
Effects of heat stress on physiological, endocrine, and reproductive functions in swine: a review
Jae-Hyeok Lee1, Se-Na Jo1, Jin-Su Kim2
1Gyeongsang National University, Jinju-si, Gyeongsangnam-do, Korea.
Abstract:
Climate change driven heat stress (HS) causes major losses in the productive and reproductive performance of swine. Using temperature-humidity index (THI) based quantification of 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. Heat stress, in the context of hypothalamic, pituitary, adrenal (HPA) sympathetic-adrenomedullary activation and insulin, catecholamine, and cortisol crosstalk, is accompanied by relative hyperinsulinemia and, via pyruvate dehydrogenase kinase 4 mediated pyruvate dehydrogenase inhibition and the lactate dehydrogenase/hypoxia-inducible factor-1α (HIF-1α) axis, repartitions substrate utilization toward glucose, thereby constraining lipid mobilization. Within the gut immune axis, β-diversity, centered dysbiosis and short chain fatty acids (SCFA) depletion weaken HIF-1α, dependent mucosal barrier defenses; together with increased lipopolysaccharide translocation, this hyperactivates TLR4/ NF-κB signaling, the NLR family pyrin domain containing 3 inflammasome, and Th17/IL-17 pathways. Evidence from fecal microbiota transplantation supports a causal role for dysbiosis in pathogenesis. In the reproductive axis, dysregulated hypothalamic-pituitary-gonadal-HPA crosstalk impairs follicular and luteal function and compromises placental nutrient transport; intrauterine HS can reprogram F1 offspring, with lasting effects on metabolism, immunity, and reproduction. In conclusion, HS is a systems level stressor that perturbs multiple physiological axes; progress will require standardized HS models, multi omics and multigenerational follow up, and integrated environment, nutrition, and management strategies. Beta diversity shifts in the gut microbiota and SCFA depletion emerge as core pathophysiologic mediators, supporting their use as early biomarkers and intervention targets and underscoring the need for focused investigation.
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