Maternal Heat Stress Alters Expression of Genes Associated with Nutrient Transport Activity and Metabolism in Female Placentae from Mid-Gestating Pigs.

Placental insufficiency is a known consequence of maternal heat stress during gestation in farm animals. The molecular regulation of placentae during the stress response is little known in pigs. This study aims to identify differential gene expression in pig placentae caused by maternal heat exposure during early to mid-gestation. RNA sequencing (RNA-seq) was performed on female placental samples from pregnant pigs exposed to thermoneutral control (CON; constant 20 °C; n = 5) or cyclic heat stress (HS; cyclic 28 to 33 °C; n = 5) conditions between d40 and d60 of gestation. On d60 of gestation, placental efficiency (fetal/placental weight) was decreased (p = 0.023) by maternal HS. A total of 169 genes were differentially expressed (FDR ≤ 0.1) between CON and HS placentae of female fetuses, of which 35 genes were upregulated and 134 genes were downregulated by maternal HS. The current data revealed transport activity (FDR = 0.027), glycoprotein biosynthetic process (FDR = 0.044), and carbohydrate metabolic process (FDR = 0.049) among the terms enriched by the downregulated genes (HS vs. CON). In addition, solute carrier (SLC)-mediated transmembrane transport (FDR = 0.008) and glycosaminoglycan biosynthesis (FDR = 0.027), which modulates placental stroma synthesis, were identified among the pathways enriched by the downregulated genes. These findings provide evidence that heat-stress induced placental inefficiency may be underpinned by altered expression of genes associated with placental nutrient transport capacity and metabolism. A further understanding of the molecular mechanism contributes to the identification of placental gene signatures of summer infertility in pigs.

Gestational heat stress alters skeletal muscle gene expression profiles and vascularity in fetal pigs in a sexually dimorphic manner.

BACKGROUND: There is evidence that sow heat stress (HS) during gestation affects fetal development with implications for impaired muscle growth. We have previously demonstrated that maternal HS during early to mid-gestation compromised muscle fibre hyperplasia in developing fetal pigs. Thus, we hypothesised these phenotypic changes are associated with a change in expression of genes regulating fetal skeletal muscle development and metabolism. To test this, at d 60 of gestation, RNA sequencing and immunohistochemistry were performed on fetal longissimus dorsi (LD) muscle biopsies collected from pregnant gilts that had experienced either thermoneutral control (CON, 20 °C, n = 7 gilts, 18 LD samples) or controlled HS (cyclic 28 to 33 °C, n = 8 gilts, 23 LD samples) conditions for 3 weeks. RESULTS: A total of 282 genes were differentially expressed between the HS and CON groups in female LD muscles (false discovery rate (FDR) ≤ 0.05), whereas no differentially expressed genes were detected in male LD muscles between the two groups (FDR > 0.05). Gestational HS increased the expression of genes associated with transcription corepressor activity, adipogenesis cascades, negative regulation of angiogenesis and pro-inflammatory signalling in female LD muscles. Immunohistochemical analyses revealed a decreased muscle vascularity density in fetuses from HS group for both sexes compared to those from the CON group (P = 0.004). CONCLUSIONS: These results reveal gilt HS during early to mid-gestation altered gene expression profiles in fetal LD muscles in a sexually dimorphic manner. The molecular responses, including transcription and angiogenesis repressions and enhanced adipogenesis cascades, were exclusively observed in females. However, the associated reductions in muscle vascularity were observed independently of sexes. Collectively this may indicate female fetal pigs are more adaptive to gestational HS in terms of gene expression changes, and/or there may be sexually dimorphic differences with respect to the timing of muscle molecular responses to gestational HS.

A Dietary Sugarcane-Derived Polyphenol Mix Reduces the Negative Effects of Cyclic Heat Exposure on Growth Performance, Blood Gas Status, and Meat Quality in Broiler Chickens.

Heat stress (HS) compromises growth performance and meat quality of broiler chickens by interrupting lipid and protein metabolism, resulting in increased oxidative damages. The experiment attempted to investigate whether dietary polyphenols (Polygain (POL)) could ameliorate the aforementioned adverse effects of HS on performance and meat quality. One hundred and twenty one day-old-male chicks were allocated to two temperature conditions, thermoneutral (TN) or HS, and fed with either a control diet (CON) or the CON plus four different doses of POL (2, 4, 6 and 10 g/kg). Heat stress caused respiratory alkalosis as evidenced by increased rectal temperature (p < 0.001) and respiration rate (p < 0.001) due to increased blood pH (p < 0.001). Heat stress decreased final body weight (p = 0.061) and breast muscle water content (p = 0.013) while POL improved both (p = 0.002 and p = 0.003, respectively). Heat stress amplified muscle damages, indicated by increased thiobarbituric acid reactive substances (p < 0.001) and reduced myofibril fragmentation index (p = 0.006) whereas POL improved both (p = 0.037 and p = 0.092, respectively). Heat stress impaired meat tenderness (p < 0.001) while POL improved it (p = 0.003). In conclusion, HS impaired growth performance and meat quality whereas POL ameliorated these responses in a dose-dependent manner, and effects of POL were evident under both temperature conditions.

Controlled elevated temperatures during early-mid gestation cause placental insufficiency and implications for fetal growth in pregnant pigs.

It is known that pig offspring born from pregnant pigs exposed to elevated ambient temperatures during gestation have altered phenotypes, possibly due to placental insufficiency and impaired fetal growth. Therefore, the objective of this study was to quantify the effect of maternal heat exposure during early-mid gestation, when pig placentae grow heavily, on placental and fetal development. Fifteen pregnant pigs were allocated to thermoneutral (TN; 20 °C; n = 7) or cyclic elevated temperature conditions (ET; 28 to 33 °C; n = 8) from d40 to d60 of gestation. Following euthanasia of the pigs on d60, placental and fetal morphometry and biochemistry were measured. Compared to TN fetuses, ET fetuses had increased (P = 0.041) placental weights and a lower (P = 0.013) placental efficiency (fetal/placental weight), although fetal weights were not significantly different. Fetuses from ET pigs had reduced (P = 0.032) M. longissimus fibre number density and a thicker (P = 0.017) placental epithelial layer compared to their TN counterparts. Elevated temperatures decreased (P = 0.026) placental mRNA expression of a glucose transporter (GLUT-3) and increased (P = 0.037) placental IGF-2 mRNA expression. In conclusion, controlled elevated temperatures between d40 to d60 of gestation reduced pig placental efficiency, resulting in compensatory growth of the placentae to maintain fetal development. Placental insufficiency during early-mid gestation may have implications for fetal development, possibly causing a long-term phenotypic change of the progeny.

Growth Performance and Characterization of Meat Quality of Broiler Chickens Supplemented with Betaine and Antioxidants under Cyclic Heat Stress.

Heat stress (HS) causes oxidative stress, which compromises broiler performance and meat quality. The aim of this study was to determine whether dietary antioxidants could be used as an amelioration strategy. Seventy-two day-old-male Ross-308 chicks were exposed to either thermoneutral or cyclical heat stress conditions. Diets were either control commercial diet (CON), CON plus betaine (BET), or with a combination of betaine, selenized yeast, and vitamin E (BET + AOX). Heat stress increased the rectal temperature (p < 0.001), respiration rate (p < 0.001), decreased blood pCO2 (p = 0.002), and increased blood pH (p = 0.02), which indicated the HS broilers had respiratory alkalosis. Final body weight was decreased by HS (p < 0.001), whereas it was improved with BET (p = 0.05). Heat stress reduced cooking loss (p = 0.007) and no effect on drip loss, while BET decreased the drip loss (p = 0.01). Heat stress reduced the myofibril fragmentation index (p < 0.001) and increased thiobarbituric acid reactive substances (p < 0.001), while these were improved with the combination of BET + AOX (p = 0.003). In conclusion, BET overall improved growth rates and product quality in this small university study, whereas some additional benefits were provided by AOX on product quality in both TN and HS broilers.