Heat stress increases insulin sensitivity in pigs

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.

Lowering rumen-degradable and rumen-undegradable protein improved amino acid metabolism and energy utilization in lactating dairy cows exposed to heat stress

“…Insulin, a potent lipolytic inhibitor, promotes lipogenesis by increasing fatty acid esterification (Vernon, 1992). Moreover, insulin promotes whole-body protein synthesis and glucose utilization in insulin-sensitive tissues (e.g., adipose and skeletal muscle; Bauman and Elliot, 1983;Sanz Fernandez et al, 2015). Although lipolysis and lipogenesis were not determined in the current study, the 10D:8U diet had greater insulin concentrations that resulted in a ~30% decrease in circulating fatty acid levels compared with lower-RDP and -RUP diets in multiparous cows.…”

“…The cause for the rise of circulating insulin is not clear during heat stress, but elevated insulin, a known promoter of glucose uptake in skeletal muscle and adipose tissues, limits fuel availability for milk synthesis during heat stress. For example, the insulin promotes glucose disposal in peripheral tissues on heat-stressed animals (Rhoads et al, 2009;Sanz Fernandez et al, 2015). Therefore, metabolic and physiological adaptations during heat stress promote the use of nutrients in peripheral tissues and may reduce nutrient availability for milk synthesis (Rhoads et al, 2009;Wheelock et al, 2010).…”

Investigating impacts of altered central metabolism on ovarian function

“…This is paradoxical to the phenotype of reduced feed intake, also a hallmark of HS [88][89][90][91][92][93]. Another apparent contradiction is that, despite hyperinsulinemia, HS was shown to increase insulin sensitivity in pigs [94] and protected rats from high-fat diet-induced insulin resistance [95]. Understanding the role of insulin in HS is crucial as it influences ovarian function (explained below).…”

Impact of endotoxemia on ovarian signaling and function

“…HS cows consume less feed but the decrease in nutrient intake only accounts for ~35-50% of milk yield decrease . During periods of HS, despite hypophagia, animals display lower levels of basal plasma non-esterified fatty acids (NEFA) , especially compared to their pair-fed thermal-neutral (TN) counterparts Sanz Fernandez et al, 2015b). Epinephrine is increased during HS (Alvarez and Johnson, 1973) and is a lipolytic signal.…”

“…Despite decreased feed intake, there is a counterintuitive effect of increased circulating insulin during HS (Hall et al, 1980;O'Brien et al, 2010;Sanz Fernandez et al, 2015b). Interestingly, Schuman (1972) noted that diabetic humans are more susceptible to heat-induced pathology.…”