Production, biological, and genetic responses to heat stress in ruminants and pigs

Abstract Text:

Heat stress (HS) compromised efficient animal production and reduced livestock output during the summer was traditionally thought to result from decreased nutrient intake. Our data from ruminants and monogastrics challenge this dogma and indicate that heat-stressed animals utilize homeorhetic strategies to modify metabolic and fuel selection priorities independently of feed intake. Systemic shifts in bioenergetics are characterized by increased basal and stimulated circulating insulin. Hepatocytes and myocytes also show clear differences in glucose production and metabolic flexibility, respectively, during HS. Intriguingly, HS animals do not mobilize adipose tissue despite being in both a negative energy balance and catabolic state. The origin of the aforementioned metabolic changes may lay at the gastrointestinal tract.  For a variety of reasons, HS compromises intestinal integrity.  Increased permeability to luminal contents results in local and systemic inflammatory responses. Consequently, heat-stressed animals are simultaneously confronted with life-threatening hyperthermia and endotoxemia.  Determining how these systems are homeostatically and homeorhetically coordinated to prioritize acclimation and survival vs. agriculturally productive purposes would presumably reveal mechanisms amenable to manipulation. Interestingly, thermoregulatory and production responses to HS are only marginally related.  In other words, increases in body temperature indices poorly predict the decrease in both milk yield and growth. Further, HS-induced decreased feed intake is also an inaccurate predictor of milk yield or growth during HS. This suggests that traits associated with production and thermoregulation during HS may be governed by separate genomic loci and potentially interdependent biological mechanisms. Thus, selecting animals with a “tolerant” phenotype based solely or separately on thermoregulatory capacity or production may not ultimately increase HS resilience. Therefore, the variation of multiple phenotypes and genotypes needs to be accounted for to generate a more comprehensive heat tolerant animal. In summary, HS is one of the primary hurdles to efficient animal production. Defining the physiological mechanisms through which HS and other environmental factors influence complex, multifactorial traits, is critical for developing approaches to ameliorate current production issues and is a prerequisite for generating future strategies (genetic, managerial, nutritional, and pharmaceutical) to maximize livestock efficiency.

Keywords: Heat stress, genetics, insulin, tolerance