Abstract
Excessive heat exposure reduces intestinal integrity and post-absorptive energetics that can inhibit wellbeing and be fatal. Therefore, our objectives were to examine how acute heat stress (HS) alters intestinal integrity and metabolism in growing pigs. Animals were exposed to either thermal neutral (TN, 21°C; 35–50% humidity; n = 8) or HS conditions (35°C; 24–43% humidity; n = 8) for 24 h. Compared to TN, rectal temperatures in HS pigs increased by 1.6°C and respiration rates by 2-fold (P<0.05). As expected, HS decreased feed intake by 53% (P<0.05) and body weight (P<0.05) compared to TN pigs. Ileum heat shock protein 70 expression increased (P<0.05), while intestinal integrity was compromised in the HS pigs (ileum and colon TER decreased; P<0.05). Furthermore, HS increased serum endotoxin concentrations (P = 0.05). Intestinal permeability was accompanied by an increase in protein expression of myosin light chain kinase (P<0.05) and casein kinase II-α (P = 0.06). Protein expression of tight junction (TJ) proteins in the ileum revealed claudin 3 and occludin expression to be increased overall due to HS (P<0.05), while there were no differences in claudin 1 expression. Intestinal glucose transport and blood glucose were elevated due to HS (P<0.05). This was supported by increased ileum Na+/K+ ATPase activity in HS pigs. SGLT-1 protein expression was unaltered; however, HS increased ileal GLUT-2 protein expression (P = 0.06). Altogether, these data indicate that HS reduce intestinal integrity and increase intestinal stress and glucose transport.
Highlights
Both humans and livestock are susceptible to high thermal loads that can cause acute, chronic, and lethal illness due to heat stressrelated pathologies
Circulating endotoxin concentrations increased 200% in heat stress (HS) pigs compared to thermal neutral (TN) counterparts (P,0.05, Figure 3)
It is important to note that nutrient restriction can lead to alterations in intestinal function, transport, morphology, and this may increase the risk of developing bacterial sepsis [26]
Summary
Both humans and livestock are susceptible to high thermal loads that can cause acute, chronic, and lethal illness due to heat stressrelated pathologies. Heat-stressed mammals partition blood to the periphery in an attempt to maximize radiant heat dissipation, and this blood redistribution is supported by vasoconstriction of the gastrointestinal tract [6]. As a result, reduced blood and nutrient flow leads to hypoxia at the intestinal epithelium, which compromises intestinal integrity and function [7]. As the gastrointestinal tract is highly sensitive to hyperthermia, and a compromised mucosa is pivotal to the pathobiology of heat - related illness, numerous animal and cell culture models have been utilized to examined the etiology of heat-induced intestinal damage [9,10,11]. Few studies have examined how high ambient temperatures affect intestinal function and integrity
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