Metabolic and health consequences of heat stress: Knowledge gaps and opportunities
Environmental-induced hyperthermia compromises efficient animal production and jeopardizes animal welfare. Reduced animal agriculture productive output during heat stress was traditionally thought to result from decreased nutrient intake. Our results in ruminants and monogastrics challenge this dogma and indicate heat-stressed animals utilize homeorhetic strategies to modify metabolic and fuel selection priorities independently of nutrient and energy intake. Systemic shifts in bioenergetics are characterized by increased basal and stimulated circulating insulin. Hepatocyte and myocyte metabolism also show clear differences in glucose production and oxidation during heat stress. Perhaps most intriguing given the energetic shortfall of the heat-stressed animal is the apparent lack of basal adipose tissue mobilization coupled with a reduced responsiveness to lipolytic stimuli. The origin of the aforementioned metabolic changes may lie at the gastrointestinal track. For a variety of reasons, heat stress compromises intestinal integrity. Increased permeability to luminal contents results in local and systemic inflammatory responses. Bacterial components might be additional signals influencing insulin secretion during heat stress. For example, in vivo lipopolysaccharide (LPS) I.V. infusion acutely increases circulating insulin in pigs and cattle, which is paradoxical as endotoxemia is a potent catabolic condition accompanied by severe pyrexia and marked hypophagia. Understanding how and why LPS induces hyperinsulinemia remains to be elucidated, but the practical implications of this phenomenon to animal agriculture are numerous. Consequently, heat-stressed animals are simultaneously confronted with life-threatening hyperthermia AND endotoxemia. However, the fields of both environmental metabolism and intestinal integrity are essentially in their infancies (especially in animal agriculture). As a result, there are numerous knowledge gaps that exist and need attention before mitigation strategies can be developed. Of particular relevance to animal agriculture are the tissue and organ specific consequences of heat stress. For example, how the liver, muscle, adipose, mammary, and ovarian systems respond to elevated temperatures, endotoxemia and LPS-induced inflammation is of obvious interest. Further, determining how these systems are homeostatically and homeorhetically coordinated to prioritize acclimation and survival vs. agriculturally productive purposes would presumably enlighten mechanisms amenable to manipulation. In summary, heat stress is one of the primary hurdles to efficient animal production. Defining the physiology and mechanisms that underlie how heat stress jeopardizes animal performance is critical for developing approaches to ameliorate current production issues and is a prerequisite for generating future strategies (genetic, managerial, nutritional, and pharmaceutical) to improve animal well-being and performance.
Keywords: Heat stress, intestinal integrity, insulin