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Effects of heat stress on post-absorptive metabolism
Heat stress (HS) jeopardizes livestock health and compromises animal productivity. Traditionally, the detrimental effects of HS have been attributed to inadequate intake. However, we have demonstrated that, given the same plane of nutrition (utilizing a pair-fed thermoneutral model, PFTN), production responses differ between thermoneutral and HS conditions in both ruminants and swine. Differences between environments indicate that HS alters post-absorptive metabolism and nutrient partitioning, independently of intake. Surprisingly, despite marked hypophagia, plasma non-esterified fatty acids (NEFA) are reduced in a variety of HS models and we have shown that heat-stressed ruminants and pigs have decreased sensitivity to lipolytic signals. Further, HS consistently increases basal insulin (a potent antilipolytic hormone), which might explain why heat-stressed animals do not mobilize NEFA. Interestingly, glucose stimulated insulin response differs between ruminants and swine, as they require more and less insulin, respectively, to dispose of glucose compared to PFTN counterparts. Reasons for such variation are not clear but might include species differences in insulin sensitivity and variations in environmental/experimental protocols. Regardless, utilizing the glucose tolerance test as a proxy for insulin sensitivity is not ideal and further research is needed to elucidate the effects of HS on insulin responsiveness. The mechanisms responsible for heat-induced changes in post-absorptive metabolism are unknown; however, they might be mediated by HS effects on intestinal health. During HS, blood flow is diverted to the periphery in an attempt to dissipate heat, leading to intestinal hypoxia, and ultimately reduced intestinal barrier function and increased leakage of luminal content (e.g. bacterial components). In agreement, in vivo lipopolysaccharide infusion results in increased plasma insulin. Additionally, prolactin might have a role on the metabolic changes observed during HS. Prolactin stimulates pancreatic β-cell proliferation and increases insulin secretion, and heat-induced hyperprolactinemia occurs in multiple species, including pigs. Finally, hyperinsulinemia and the blunted NEFA response might be the result of decreased energetic requirements during HS. Environmental hyperthermia is thought to elevate maintenance requirements, due to increased energy utilization in heat dissipation and greater chemical reaction rates. However, we observed an immediate and sustained decrease in thyroid hormones in heat-stressed pigs, which might indicate a decrease in energy expenditure/heat production. In summary, HS alters post-absorptive metabolism and nutrient partitioning independently of nutrient intake. Understanding the biology of how HS compromises animal agriculture is critical in order to develop mitigating strategies to overcome the production losses experienced during the hot summer months.
Keywords: Heat stress, Nutrient partitioning