Part 1: heat stress and the gut barrier–nutrient transporter interactions in poultry: mechanistic insights and integrated pathophysiology

SUMMARYHeat stress (HS) is a major environmental challenge in modern poultry production, adversely affecting growth performance, feed efficiency, egg production, and metabolic homoeostasis. Although systemic thermoregulatory and endocrine responses to HS are well recognised, increasing evidence indicates that the intestine plays a central mechanistic role in mediating HS-induced reductions in nutrient utilisation and productivity. This review integrates current evidence within a gut barrier–microbiota–nutrient transporter framework to clarify the complex pathophysiology of HS in poultry. Heat exposure induces splanchnic hypoperfusion, epithelial hypoxia, oxidative imbalance, and structural alterations in the intestinal mucosa, including villus shortening, crypt remodelling, and tight junction disruption. These effects increase intestinal permeability, promote inflammation, and contribute to microbial dysbiosis and altered metabolite production. Within this compromised epithelial environment, nutrient transporter systems undergo coordinated but highly context-dependent modulation. Chronic or cyclic HS is frequently associated with reduced expression or impaired function of key carbohydrate transporters such as sodium-dependent glucose cotransporter 1 (SGLT1) and glucose transporter 2 (GLUT2). In contrast, peptide transporters (PepT1 and PepT2), amino acid transporters including excitatory amino acid transporter 3 (EAAT3), and lipid transport-related proteins such as cluster of differentiation 36 (CD36), fatty acid transport proteins (FATPs), and fatty acid-binding proteins (FABPs) exhibit variable responses depending on intestinal segment, HS severity and duration, and experimental conditions. Similar alterations occur in mineral transport pathways, reflecting broader disturbances in epithelial ion homoeostasis. Current evidence supports a multilevel model in which barrier dysfunction, microbial imbalance, and transporter dysregulation collectively impair nutrient flux and metabolic efficiency under HS conditions. Thus, the gut barrier–microbiota–nutrient transporter network emerges as an integrated systems-level mechanism linking thermal stress to compromised absorptive capacity and reduced poultry productivity. These findings further highlight the importance of nutritional, microbiota-targeted, and environmental strategies to preserve intestinal integrity and transporter function during HS exposure.