Abstract

Heat stress (HS) increases circulating prolactin (PRL) in a variety of animal models (reasons remain unknown), but whether or not HS elevates PRL in growing pigs is ill‐defined. Crossbred gilts (77±2 kg) were housed in individual pens and allocated to treatments: 1) HS conditions (36°C; 50% humidity) and ad libitum feeding (n=13) or 2) thermo‐neutral (TN) conditions (19°C; 61% humidity) and pair‐feeding (n=16) to eliminate the confounding effects of dissimilar feed intake. Pigs were sacrificed at d1 or 7 of environmental exposure. Rectal temperatures (Tr) and respiratory rates (RR) were obtained 4X daily and blood and intestinal tissues harvested at death. HS pigs had increased Tr (P<0.01; 40.1 vs. 38.4°C), RR (P<0.01; 111 vs. 36 bpm) and reduced feed intake (P<0.05; 57%). By design, TN pigs’ intake mirrored the HS pattern. PRL was higher (P<0.05) in HS pigs (0.97 vs. 0.64 ng/ml). In acute HS (24 h), PRL was negatively correlated with feed intake (r = −0.71; P<0.05), ileal transepithelial resistance (TER; r = −0.85; P<0.01) and tended to be negatively correlated with colonic TER (r = −0.69; P=0.06). In chronic HS (d7), PRL tended to be only inversely correlated with glucose (r = −0.81; P<0.10). In TN pigs, PRL was not correlated with any of the measured variables. Together, PRL appears to participate in both the acute HS response and the acclimation to chronic environmental hyperthermia.Heat stress, prolactinUSDA/AFRI

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