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.

Keywords: Heat Stress; insulin sensitivity; metabolism; pig.

Figure 1

Effects of ad libitum feed intake in constant heat stress conditions (HS; 32°C) and pair-feeding in thermoneutral conditions (PFTN; 20°C) on plasma (A) glucose, (B) insulin, (C) C-peptide, (D) nonesterified fatty acids (NEFA); (E) rate of glucose infusion (ROGI); and (F) ROGI to euglycemic glucose concentration ratio in response to a hyperinsulinemic euglycemic clamp (HEC). Metabolites’ responses were calculated as the difference between the clamped and the baseline periods of the HEC. On period 1 (P1) all pigs were fed ad libitum in thermoneutral conditions. On period 2 (P2) pigs were exposed to either HS or PFTN. ^{a, b}Means with different letters differ (P ≤ 0.05)

Figure 2

Effects of ad libitum feed intake in constant heat stress conditions (HS; 32°C) and pair-feeding in thermoneutral conditions (PFTN; 20°C) on the adipose tissue protein abundance of (A) insulin receptor substrate-1 (IRS-1), (B) protein kinase B (Akt), (C) phospho-Ser Akt, and (D) phospho-Ser Akt to total Akt ratio in response to an insulin tolerance test. Tissue biopsies were obtained prior (I-) and 15 minutes after (I+) an intravenous insulin dose (0.1 U˙kg BW⁻¹).

Figure 3

Effects of ad libitum feed intake in constant heat stress conditions (HS; 32°C) and pair-feeding in thermoneutral conditions (PFTN; 20°C) on the skeletal muscle (longissimus dorsi) protein abundance of (A) insulin receptor substrate-1 (IRS-1), (B) phospho-Tyr IRS-1, (C) phospho-Tyr to total IRS-1 ratio, (D) protein kinase B (Akt), (E) phospho-Ser Akt, and (F) phospho-Ser to total Akt ratio in response to an insulin tolerance test. Tissue biopsies were obtained prior (I-) and 15 min after (I+) an intravenous insulin dose (0.1 U kg BW⁻¹). ^{a, b}Means with different superscripts differ (P ≤ 0.05).