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. 2025 Jul 23;15(1):26730.
doi: 10.1038/s41598-025-12698-w.

Early gestation heat stress influences fetal biomarkers indicative of maternal cortisol transfer in pigs

MaryKate H Byrd  1 , L Kirsten Senn  1 , Alex Pasternak  1 , Kara R Stewart  1 , Jay S Johnson  2
Affiliations

Early gestation heat stress influences fetal biomarkers indicative of maternal cortisol transfer in pigs

MaryKate H Byrd et al. Sci Rep. .

Abstract

In utero heat stress (IUHS) alters hypothalamic-pituitary-adrenal (HPA) axis development in pigs; however, the mechanisms mediating this effect remain unclear. This study aimed to evaluate cortisol transfer dynamics from the heat-stressed (HS) dam to the IUHS conceptus during early gestation. We hypothesized that gestational HS would modify maternal cortisol secretion and increase conceptus cortisol exposure. Twenty-three gilts were exposed to thermoneutral (TN; n = 11) or HS (n = 12) conditions from gestation d 6 to 33. Maternal vaginal temperature, respiration rate, skin temperatures, and salivary cortisol concentrations were monitored. On d 33, dams were harvested to assess fetal and reproductive tract morphology and collect fetal and placental samples for glucocorticoid and 11β-HSD2 analyses. Heat-stressed gilts exhibited increased (P ≤ 0.01) vaginal temperature, respiration rate, and skin temperatures, but salivary cortisol was similar (P = 0.13). Total and viable fetuses per corpus luteum were reduced (P ≤ 0.05) in HS dams. Fetal tissue cortisone: cortisol tended to be reduced (P = 0.06) and was reduced in IUHS fetus amniotic fluid (P = 0.03). Amniotic fluid cortisone tended to decrease (P = 0.07), while cortisol tended to increase (P = 0.08) in IUHS fetuses. These data suggest IUHS increases fetal glucocorticoid exposure.

Keywords: In utero heat stress; 11β-HSD2; Fetal cortisol; Fetal cortisone; Maternal cortisol.

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Conflict of interest statement

Declarations. Competing interests: The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Diagram illustrating the reproductive tract regions where fetuses (including the placenta, fetus, and amniotic fluid) were collected. The uterine horns were divided into two distinct regions, denoted by dashed lines, and the median fetus was identified and selected, as indicated by brackets labeled A, B, C, and D. Figure created in Biorender.com.
Fig. 2
Fig. 2
The effects of early gestation (d 6.0 ± 0.7 to d 33.0 ± 1.7) heat stress (HS) or thermoneutral (TN) conditions on gilt vaginal temperature (TV) by study day. An asterisk (*) indicates overall differences (P < 0.01) by environmental treatment. Letters (a, b) denote environmental treatment by study day differences (P = 0.02). Data are presented as LSmeans ± SE.
Fig. 3
Fig. 3
The effects of early gestation (d 6.0 ± 0.7 to d 33.0 ± 1.7) heat stress (HS) or thermoneutral (TN) conditions on gilt respiration rate (RR) by study day. An asterisk (*) indicates overall differences (P < 0.01) by environment treatment. Letters (a, b) indicate environmental treatment by study day differences (P < 0.01). Data are presented as LSmeans ± SE.
Fig. 4
Fig. 4
The effects of early gestation (d 6.0 ± 0.7 to d 33.0 ± 1.7) heat stress (HS) or thermoneutral (TN) conditions on gilt (A) ear skin temperature (Tear) and (B) rump skin temperature (Trump) by study day. An asterisk (*) indicates overall differences (P < 0.01) by environment treatment. Letters (a, b) indicate environmental treatment by study differences (P < 0.01). Data are presented as LSmeans ± SE.
Fig. 5
Fig. 5
The effects of early gestation (d 6.0 ± 0.7 to d 33.0 ± 1.7) heat stress (HS) or thermoneutral (TN) conditions on gilt body weight (BW) by study day. Letters (a, b, c, d) indicate environmental treatment by study day differences (P < 0.01). Data are presented as LSmeans ± SE.
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