Abstract
Proper insulin homeostasis appears critical for adapting to and surviving a heat load. Further, heat stress (HS) induces phenotypic changes in livestock that suggest an increase in insulin action. The current study objective was to evaluate the effects of HS on whole-body insulin sensitivity. Female pigs (57 ± 4 kg body weight) were subjected to two experimental periods. During period 1, all pigs remained in thermoneutral conditions (TN; 21°C) and were fed ad libitum. During period 2, pigs were exposed to: (i) constant HS conditions (32°C) and fed ad libitum (n = 6), or (ii) TN conditions and pair-fed (PFTN; n = 6) to eliminate the confounding effects of dissimilar feed intake. A hyperinsulinemic euglycemic clamp (HEC) was conducted on d3 of both periods; and skeletal muscle and adipose tissue biopsies were collected prior to and after an insulin tolerance test (ITT) on d5 of period 2. During the HEC, insulin infusion increased circulating insulin and decreased plasma C-peptide and nonesterified fatty acids, similarly between treatments. From period 1 to 2, the rate of glucose infusion in response to the HEC remained similar in HS pigs while it decreased (36%) in PFTN controls. Prior to the ITT, HS increased (41%) skeletal muscle insulin receptor substrate-1 protein abundance, but did not affect protein kinase B or their phosphorylated forms. In adipose tissue, HS did not alter any of the basal or stimulated measured insulin signaling markers. In summary, HS increases whole-body insulin-stimulated glucose uptake.
Highlights
Heat stress (HS) is a major environmental hazard for both humans and animals
Feed intake acutely decreased (40%) at the beginning of period 2, reached its minimum on day 3, and increased thereafter without recovering to the period 1 feed intake (FI) level (P < 0.01; Table 1)
At the beginning of period 2, basal plasma nonesterified fatty acids (NEFA) acutely increased for both treatments, peaked on day 3, and sharply decreased thereafter (P < 0.01); but overall, HS pigs had decreased circulating NEFA (46%; P < 0.01) compared to PFTN controls (Table 2)
Summary
Despite advances in the understanding of heat-related illnesses, there is no treatment against specific aspects of their pathophysiology, and protocols are limited to generic cooling and rehydration (Leon and Helwig 1985). A better understanding of the biological consequences of HS is critical in order to develop effective treatment protocols and mitigation strategies. Diabetic humans and rodents are more susceptible to heat-related illnesses, and exogenous insulin rescues this phenotype (Semenza et al 1999; Niu et al.2003). Thermal therapy improves insulin sensitivity in diabetic and obese rodents and humans (Hooper 1999; Kokura et al 2007; Gupte et al 2009). We have previously reported that, despite hypercatabolic hallmarks including marked hypophagia and weight loss, HS increases basal and stimulated circulating insulin and decreases adipose tissue mobilization in a variety of species (Baumgard and Rhoads 2013), including pigs (Pearce et al 2013a; Sanz Fernandez et al 2015)
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