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Study objectives were to evaluate the effects of mitoquinol (MitoQ) on production parameters, gastrointestinal tract (GIT ; stomach and small and large intestines) weight, and circulating leukocytes during a 24-h acute heat stress (HS) challenge. Crossbred gilts [ n  = 32; 49.1 ± 2.4 kg body weight (BW)] were blocked by BW and randomly assigned to 1 of 4 environmental-therapeutic treatments: 1) thermoneutral (TN) control (n  = 8; TNCON), 2) TN and MitoQ (n  = 8; TNMitoQ), 3) HS control (n  = 8; HSCON), or 4) HS and MitoQ (n  = 8; HSMitoQ). Pigs were moved into individual pens and allowed to acclimate for 6 d. The study consisted of 2 experimental periods (P). During P1 (2 d), all pigs remained in TN conditions (20.6 ± 1.5 °C) and were fed ad libitum. During P2 (24 h), pigs were fed ad libitum and exposed to either TN or constant HS (37.3 ± 1.3 °C). Mitoquinol (40 mg/d) was orally administered twice daily (0700 and 1800 hours) during P1 and P2. As expected, pigs exposed to HS had increased rectal temperature, skin temperature, and respiration rate (+1.5 °C, +8.7 °C, and +86 bpm, respectively; P  < 0.01) compared to their TN counterparts. Compared to TN, HS pigs had decreased feed intake (67%; P  < 0.01) and significant BW loss (+1.5 vs. −1.9 kg, respectively; P  < 0.01). Total GIT weight was decreased in HS relative to TN pigs (P  < 0.01), and this was influenced by decreased luminal contents (2.43 vs. 3.26 kg, respectively; P  < 0.01) and reduced empty GIT mass (3.21 vs. 3.48 kg, respectively; P  = 0.03). Stomach contents remained similar between TN and HS pigs (P  > 0.54) but tended to increase in MitoQ relative to CON pigs (0.90 vs. 0.63 kg, respectively; P  = 0.08). Stomach content as a percentage of the previous 24 h feed intake was increased in HS compared to the TN controls (93% vs. 31%; P  < 0.01). In contrast, small and large intestinal contents were decreased in HS compared to TN pigs (23% and 49%, respectively; P  < 0.01). Liver weight decreased in HS relative to TN pigs (1.15 vs. 1.22 kg, respectively; P  = 0.02), and was decreased in MitoQ compared to CON pigs (1.13 vs. 1.24 kg; P  < 0.01). Circulating lymphocytes tended to be decreased in HS relative to TN pigs (16%; P  = 0.07). In summary, acute HS increased all body temperature indices, negatively influenced animal performance, and differentially altered GIT motility as evidenced by decreased gastric emptying and increased intestinal transit. However, MitoQ supplementation did not appear to ameliorate these effects. [ABSTRACT FROM AUTHOR]

Study objectives were to characterize the effects of citrulline (CIT) on physiological and intestinal morphology metrics during heat stress (HS) and feed restriction. Forty crossbred gilts (30 ± 2 kg body weight [BW]) were assigned to one of five treatments: (1) thermoneutral (TN) fed ad libitum (AL) with control (CON) supplement (TNAL; n  = 8), (2) TN pair-fed (PF) with CON (PF-CON; n  = 8), (3) TN PF with CIT (PF-CIT; n  = 8), (4) HS AL with CON (HS-CON; n  = 8), and (5) HS AL with CIT (HS-CIT; n  = 8). During the period (P) 1 (7 d), pigs were in TN conditions (23.6 °C) and fed AL their respective supplemental treatments. During P2 (2.5 d), HS-CON and HS-CIT pigs were fed AL and exposed to cyclical HS (33.6 to 38.3 °C), while TNAL, PF-CON, and PF-CIT remained in TN and were fed either AL or PF to their HS counterparts. Citrulline (0.13 g/kg BW) was orally administered twice daily during P1 and P2. HS increased rectal temperature (Tr), skin temperature (Ts), and respiration rate (RR) relative to TN pigs (0.8 °C, 4.7 °C, and 47 breaths/min, respectively; P  < 0.01). However, HS-CIT had decreased RR (7 breaths/min, P  = 0.04) and a tendency for decreased Tr (0.1 °C, P  = 0.07) relative to HS-CON pigs. During P2, HS pigs had decreased feed intake (22%; P  < 0.01) and a tendency for decreased average daily gain (P  = 0.08) relative to TNAL pigs, and by experimental design, PF pigs followed this same pattern. Circulating lipopolysaccharide-binding protein tended to be decreased (29%; P  = 0.08) in PF relative to TNAL pigs and was increased (41%; P  = 0.03) in HS compared to PF pigs. Jejunum villus height was decreased in PF relative to TNAL pigs (15%; P  = 0.03); however, CIT supplementation improved this metric during feed restriction (16%; P  = 0.10). Jejunum mucosal surface area decreased in PF (16%; P  = 0.02) and tended to decrease in HS (11%; P  = 0.10) compared to TNAL pigs. Ileum villus height and mucosal surface area decreased in HS compared to TNAL pigs (10 and 14%, respectively; P  ≤ 0.04), but both parameters were rescued by CIT supplementation (P  ≤ 0.08). Intestinal myeloperoxidase and goblet cell area remained similar among treatments and intestinal segments (P  > 0.24). In summary, CIT supplementation slightly improved RR and Tr during HS. Feed restriction and HS differentially affected jejunum and ileum morphology and while CIT ameliorated some of these effects, the benefit appeared dependent on intestinal section and stressor type. [ABSTRACT FROM AUTHOR]

Zearalenone (ZEN), a nonsteroidal estrogenic mycotoxin, causes endocrine disruption and porcine reproductive dysfunction. Heat stress (HS) occurs when exogenous and metabolic heat accumulation exceeds heat dissipation. Independently, HS and ZEN both compromise swine reproduction; thus, the hypothesis investigated was two-pronged: that ZEN exposure would alter the ovarian proteome and that these effects would differ in thermal neutral (TN) and HS pigs. Pre-pubertal gilts (n  = 38) were fed ad libitum and assigned to either (TN: 21.0 ± 0.1 °C) or HS (12 h cyclic temperatures of 35.0 ± 0.2 °C and 32.2 ± 0.1 °C). Within the TN group, a subset of pigs were pair-fed (PF) to the amount of feed that the HS gilts consumed to eliminate the confounding effects of dissimilar nutrient intake. All gilts orally received a vehicle control (CT) or ZEN (40 μg/kg/BW) resulting in six treatment groups: thermoneutral (TN) vehicle control (TC; n  = 6); TN ZEN (TZ; n  = 6); PF vehicle control (PC; n  = 6); PF ZEN (PZ; n  = 6); HS vehicle control (HC; n  = 7); or HS ZEN (HZ; n  = 7) for 7 d. When compared to the TC pigs, TZ pigs had 45 increased and 39 decreased proteins (P  ≤   0.05). In the HZ pigs, 47 proteins were increased and 61 were decreased (P  ≤   0.05). Exposure to ZEN during TN conditions altered sec61 translocon complex (40%), rough endoplasmic reticulum membrane (8.2%), and proteasome complex (5.4%), asparagine metabolic process (0.60%), aspartate family amino acid metabolic process (0.14%), and cellular amide metabolic process (0.02%) pathways. During HS, ZEN affected cellular pathways associated with proteasome core complex alpha subunit complex (0.23%), fibrillar collagen trimer (0.14%), proteasome complex (0.05%), and spliceosomal complex (0.03%). Thus, these data identify ovarian pathways altered by ZEN exposure and suggest that the molecular targets of ZEN differ in TN and HS pigs. [ABSTRACT FROM AUTHOR]

The influence of systemic immune activation on whole-body calcium (Ca) trafficking and gastrointestinal tract (GIT) physiology is not clear. Thus, the study objectives were to characterize the effects of lipopolysaccharide (LPS) on Ca pools and GIT dynamics to increase understanding of immune-induced hypocalcemia, ileus, and stomach hemorrhaging. Twelve crossbred pigs [44 ± 3 kg body weight (BW)] were randomly assigned to 1 of 2 intramuscular treatments: (1) control (CON ; 2 mL saline; n  = 6) or (2) LPS (40 µg LPS/kg BW; n  = 6). Pigs were housed in metabolism stalls to collect total urine and feces for 6 h after treatment administration, at which point they were euthanized, and various tissues, organs, fluids, and digesta were weighed, and analyzed for Ca content. Data were analyzed with the MIXED procedure in SAS 9.4. Rectal temperature and respiration rate increased in LPS relative to CON pigs (1.4 °C and 32%, respectively; P  ≤ 0.05). Inflammatory biomarkers such as circulating alkaline phosphatase, aspartate aminotransferase, and total bilirubin increased in LPS compared with CON pigs whereas albumin decreased (P  ≤ 0.02). Plasma glucose and urea nitrogen decreased and increased, respectively, after LPS (43% and 80%, respectively; P  < 0.01). Pigs administered LPS had reduced circulating ionized calcium (iCa) compared to CON (15%; P  < 0.01). Considering estimations of total blood volume, LPS caused an iCa deficit of 23 mg relative to CON (P  < 0.01). Adipose tissue and urine from LPS pigs had reduced Ca compared to CON (39% and 77%, respectively; P  ≤ 0.05). There did not appear to be increased Ca efflux into GIT contents and no detectable increases in other organ or tissue Ca concentrations were identified. Thus, while LPS caused hypocalcemia, we were unable to determine where circulating Ca was trafficked. LPS administration markedly altered GIT dynamics including stomach hemorrhaging, diarrhea (increased fecal output and moisture), and reduced small intestine and fecal pH (P  ≤ 0.06). Taken together, changes in GIT physiology suggested dyshomeostasis and alimentary pathology. Future research is required to fully elucidate the etiology of immune activation-induced hypocalcemia and GIT pathophysiology. [ABSTRACT FROM AUTHOR]

Heat stress (HS) occurs when exogenous and metabolic heat accumulation exceeds heat dissipation; a thermal imbalance that compromises female reproduction. This study investigated the hypothesis that HS alters the ovarian proteome and negatively impacts proteins engaged with insulin signaling, inflammation, and ovarian function. Prepubertal gilts (n  = 19) were assigned to one of three environmental groups: thermal neutral with ad libitum feed intake (TN ; n  = 6), thermal neutral pair-fed (PF ; n  = 6), or HS (n  = 7). For 7 d, HS gilts were exposed to 12-h cyclic temperatures of 35.0 ± 0.2 °C and 32.2 ± 0.1 °C, while TN and PF gilts were housed at 21.0 ± 0.1 °C. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was performed on ovarian protein homogenates. Relative to TN gilts, 178 proteins were altered (P  ≤   0.05, log2foldchange   ≥ 1) by HS, with 76 increased and 102 decreased. STRING gene ontology classified and identified 45 biological processes including those associated with chaperone protein refolding, cytoplasmic translational initiation, and immune activation; with a protein–protein interaction web network of 158 nodes and 563 edges connected based on protein function (FDR ≤ 0.05). Relative to PF, HS altered 330 proteins (P  ≤   0.05, log2foldchange   ≥ 1), with 151 increased and 179 decreased. Fifty-seven biological pathways associated with protein function and assembly, RNA processing, and metabolic processes were identified, with a protein–protein interaction network of 303 nodes and 1,606 edges. Comparing HS with both the TN and PF treatments, 72 ovarian proteins were consistently altered by HS with 68 nodes and 104 edges, with biological pathways associated with translation and gene expression. This indicates that HS alters the ovarian proteome and multiple biological pathways and systems in prepubertal gilts; changes that potentially contribute to female infertility. [ABSTRACT FROM AUTHOR]

Objectives were to evaluate the effects of mitoquinol (MitoQ) on production parameters, gastrointestinal (GIT) contents, GIT mass, and circulating leukocytes during acute heat stress (HS). Crossbred gilts [49.1±2.4 kg body weight (BW)] were blocked by BW and randomly assigned to 1 of 4 therapeuticenvironmental treatments: 1) thermoneutral (TN) control (TNCON; n = 8), 2) TN and MitoQ (TNMitoQ; n = 8), 3) HS control (HSCON; n = 8), or 4) HS and MitoQ (HSMitoQ; n = 8). The study consisted of two experimental periods (P). During P1 (2 d) pigs were fed ad libitum and housed in TN conditions (20.6±1.5°C). During P2 (24 h) pigs were fed ad libitum and exposed to either TN or constant HS (37.3±1.3°C). In MitoQ fed pigs, MitoQ (20 mg) was administered twice daily (0700 and 1800 h; 40 mg/d) during both P1 and P2. Rectal temperature (TR), skin (TS), respiration rate (RR), and feed intake (FI) were recorded every 4 h during P2. Following P2, all pigs were euthanized, and organs were weighed. As expected, pigs exposed to HS had increased TR, TS, and RR (1.5°C, 8.7°C, and 86 bpm, respectively; P < 0.01) relative to TN. Compared with TN, HS pigs had decreased FI (67%; P < 0.01). Additionally, HS pigs lost BW compared with TN (-1.9 vs. +1.5 kg, respectively; P < 0.01). Despite consuming 67% less feed, stomach contents were similar in TN and HS pigs (P > 0.54), regardless of environment. Large and small intestine contents were decreased in HS pigs relative to TN (23 and 49%, respectively; P = 0.01). Total GIT luminal contents (stomach, small and large intestines) were decreased in HS relative to TN pigs (2.43 vs. 3.26 kg; P = 0.01); however, MitoQ fed pigs tended to have increased GIT contents regardless of the environment (3.05 vs. 2.63 kg; P = 0.08). Total empty GIT and liver weights decreased in HS relative to TN pigs (3.21 vs. 3.48 and 1.16 vs. 1.22 kg, respectively; P = 0.03). In addition, liver weight was decreased in MitoQ relative to CON pigs (1.13 vs. 1.24 kg; P = 0.01). Further, total GIT weight (tissue and contents) was decreased in HS relative to TN pigs (5.63 vs. 6.70 kg; P = 0.01). Environment nor therapeutic treatment affected circulating leukocytes (P > 0.16); however, HS pigs tended to have decreased lymphocytes relative to TN (16%; P = 0.07). Based upon the changes in GIT content, it appears HS decreases gastric emptying while increasing intestinal passage rate. Overall, acute HS increased body temperature indices, and decreased FI, GIT mass and BW; however, MitoQ administration did not appear to ameliorate these metrics. [ABSTRACT FROM AUTHOR]

Study objectives were to determine the effects of chromium (Cr) propionate (Cr propionate 0.04%; 0.5 g/kg of feed to deliver 200 parts per billion Cr/d; KemTRACE Cr, Kemin Industries, Inc. Des Moines, IA) on growth performance, metabolism, and health biomarkers in heat-stressed and nutrient-restricted pigs. Crossbred barrows (n = 96; 105 ± 1 kg BW) were enlisted in an experiment conducted in two replicates, blocked by initial BW, and randomly assigned to one of six dietary-environmental treatments: (i) thermoneutral (TN) and fed ad libitum a control diet (TNCtl), (ii) TN and fed ad libitum a Cr supplemented diet (TNCr), (iii) TN and pair-fed a control diet (PFCtl), (iv) TN and pair-fed a Cr supplemented diet (PFCr), (v) heat stress (HS) and ad libitum fed a control diet (HSCtl), or (vi) HS and ad libitum fed a Cr supplemented diet (HSCr). The study consisted of three experimental periods (P). During P0 (5 d), all pigs were housed in TN conditions (21.3 ± 0.1 °C, 56.8 ± 0.3% relative humidity [ RH ]) and fed the control diet ad libitum. During P1 (5 d), pigs were fed their respective dietary treatments ad libitum and kept in TN conditions. During P2 (35 d), HSCtl and HSCr-treated pigs were fed ad libitum and exposed to progressive cyclical HS conditions (27 to 31 °C, 50 ± 0.3% RH), while TNCtl, TNCr, PFCtl, and PFCr pigs remained in TN conditions and were fed ad libitum or pair-fed to their respective HSCtl and HSCr counterparts to eliminate the confounding effects of dissimilar feed intake. Overall, HS pigs had increased (P < 0.01) rectal temperature, skin temperature, and respiration rate (0.3 °C, 3.8 °C, and 32 breaths per minute, respectively) relative to TN pigs. Overall, HS decreased ADFI and ADG (20 and 21%, respectively; P < 0.01) compared with TN controls. Final BW tended to be increased in HSCr (2.7 kg, P = 0.06) compared with HSCtl pigs. Similarly, ADG tended to be increased during P2 in HSCr relative to HSCtl-treatment (0.77 vs. 0.72 kg/d; P = 0.10). There were no effects of Cr on most production parameters, but ADFI tended to be increased in Cr relative to Ctl-fed pigs (3.19 vs. 3.09 kg/d; P = 0.08). No effects of Cr supplementation were detected on circulating glucose, insulin, NEFA, cholesterol, triglycerides, or lipopolysaccharide binding protein. However, blood neutrophils were increased in HSCr (37%; P < 0.01) relative to HSCtl pigs. In summary, these results suggest Cr supplementation may benefit growth performance during HS. [ABSTRACT FROM AUTHOR]

Heat stress (HS) jeopardizes animal productivity and health. The intestinal barrier is sensitive to HS and heat-induced hyperpermeability plays a key role in its pathophysiology. However, the biology of recovery following HS is less understood. Thus, study objectives were to determine the temporal pattern of metabolic, inflammatory, and intestinal histological parameters during HS recovery. Female pigs (n = 32; 19.5 ± 0.5 kg BW) were sacrificed following exposure to 1 of 4 environmental treatments: 1) constant thermoneutral (TN) conditions (TNC; 24.2 ± 0.5°C), 2) no TN recovery post HS (0D), 3) 3 d of TN recovery post HS (3D), and 4) 7 d of TN recovery post HS (7D). The HS protocol was cyclical (33.6 ± 1.8 to 37.4 ± 2.1°C) and lasted for 3 d for all HS treatments. During the 3 d of HS, rectal temperature, skin temperature, and respiration rates were increased (1.3°C, 4.8°C, and 77 breaths/min, respectively; P < 0.01) and ADFI was decreased (27%; P < 0.01) compared to TNC pigs. Skin temperature tended to be decreased 0.6°C in 3D pigs during days 1–3 of recovery (P = 0.06) and was decreased 1.6 and 0.7°C during days 1–3 and 4–7 of recovery, respectively, in 7D pigs (P ≤ 0.03) compared to TNC. Relative to TNC pigs, ADFI remained 14% decreased during days 1–3 of recovery in both 3D and 7D pigs, and 17% decreased during days 4–7 in 7D pigs (P ≤ 0.01). Plasma glucose was decreased (10%; P = 0.03) for 0D and 3D relative to TNC pigs. Circulating lipopolysaccharide-binding protein was increased in 3D and 7D vs. TNC pigs (110 and 147%, respectively; P = 0.01) and tended to increase linearly with increasing recovery time (P = 0.08). Circulating tumor necrosis factor alpha was decreased (15%) in 0D pigs and increased linearly with advancing recovery time (P < 0.01). Jejunum and ileum villus height were reduced 17 and 11% in 0D vs. TNC pigs and increased linearly with progressive recovery time (P < 0.01). Jejunum and ileum mucosal surface areas were reduced 17 and 9% in 0D pigs and remained decreased in the jejunum while the ileum recovered to TNC levels by day 3 of recovery. Relative to TNC pigs, goblet cell area was similar in jejunum and colon of 0D pigs but was reduced in the ileum of 0D pigs and in jejunum, ileum, and colon of 3D and 7D relative to TNC pigs (P < 0.01). In summary, HS has deleterious effects on intestinal morphology that seem to improve with recovery time. In contrast, feed consumption remained suppressed and inflammatory biomarkers indicative of leaky gut increased following the heat load. [ABSTRACT FROM AUTHOR]

Heat stress can negatively impact pig health and performance but the effects of heat stress on skeletal muscle mitochondrial function are largely unknown. We hypothesized that mitochondrial function and capacity would be impaired in heat stressed (HS) compared to thermoneutral (TN) pigs but mitochondrially-targeted coenzyme Q (MitoQ) supplementation would rescue the impairment. Oxidative portions of the semitendinosus muscle were evaluated from TN and HS gilts receiving no supplementation (CON) or MitoQ for 2 d prior to and during the 24h environmental heat treatment (n = 8 per group). Mitochondrial oxidative phosphorylation (P) and electron transfer (E) capacities were determined via high resolution respirometry and mitochondrial volume density and function were quantified by citrate synthase (CS) and cytochrome c oxidase activities, respectively. Data were analyzed using linear models in SAS v9.4 with fixed effects of heat, MitoQ treatment (trt), and heat×trt interaction. There were trends for the interaction of trt and heat (P≤0.1) on integrative (per mg tissue) and intrinsic (relative to CS) P with complexes I and II (PCI+II), maximum noncoupled E (ECI+II), and E with complex II only (ECII), in which all measures were greater in HS-MitoQ than TN-MitoQ (P≤0.03), but measures did not differ due to HS in CON pigs. The contribution of leak to total E (flux control ratio, FCRLeak) was lesser in HS-MitoQ than HS-CON, TN-CON, and TN-MitoQ (P≤0.02). The FCRPCI was greater (P≤0.05) while the FCRPCI+II was lesser (P=0.01) in TN compared to HS pigs. Finally, the FCRPCI+II was greater (P=0.02) while the FCRECII tended to be lesser (P=0.09) for CON than MitoQ pigs. Neither mitochondrial volume density nor function were affected by HS or MitoQ supplementation. In total, these data indicate improved mitochondrial capacities following heat stress in pigs receiving MitoQ but no difference in mitochondrial capacities in unsupplemented, HS pigs. [ABSTRACT FROM AUTHOR]

Zearalenone (ZEA), an estrogenic mycotoxin, causes hormonal disruption and reproductive dysfunction in pigs. Heat stress (HS) occurs when exogenous and metabolic heat accumulation exceeds heat dissipation; a scenario negatively impacting gilt reproduction. Our objective was to identify differentially abundant ovarian proteins in gilts exposed to HS +/- ZEA. We hypothesized that ZEA exposure would negatively impact the prepubertal gilt ovarian proteome and HS would be additive to ZEA-induced toxicity. Prepubertal gilts (n = 38) were assigned to one of six treatment groups: thermoneutral (TN) ad libitum control (TNCtl; n = 6); TN + ZEA (TNZea; 2 ppm; n = 6); pair-fed (PF) control (PFCtl; n = 6); PF+ ZEA (PFZea; 2 ppm; n = 6); cyclical HS control (HSCtl; n = 7); and HS + ZEA (HSZea; 2 ppm; n = 7). Gilts were subjected to TN (20 ± 1°C) or cyclic HS (35 ± 1°C for 12 h/31.6° for 12 h) conditions for 7 d. Liquid chromatography-mass spectrometry (LC-MS/MS) was performed on ovarian protein homogenates. Exposure to ZEA altered (P < 0.05) abundance of 93 proteins in TN gilts (48 increased and 45 decreased). In PF gilts, ZEA increased 50 and decreased 47 proteins (P < 0.05). During HS, ZEA differentially affected (P < 0.05) 126 proteins: 58 increased and 68 increased. Pathways impacted by either HS or ZEA alone or in combination included cellular stress, metabolic pathways, and estrogenic pathways. Thus, ZEA and HS, either alone or in combination, impact the ovarian proteome in prepubertal gilts in ways that could contribute to seasonal infertility. This project was supported by the Iowa Pork Producers Association. [ABSTRACT FROM AUTHOR]

Seasonal infertility (SI) caused by heat stress (HS) impacts the US swine industry by reducing litter size, farrowing rates, and production efficiency. Identifying the biological underpinnings of SI is a foundational step towards developing mitigation strategies to reduce the nearly $1 billion annual revenue losses to the swine industry. The study objective was to investigate the direct and indirect effects of HS via HS conditioned serum infusion in swine. We hypothesized gilts housed in thermoneutral (TN) conditions receiving gradual infusions of serum obtained from HS gilts would experience altered endocrine and metabolic function compared to gilts receiving serum from TN gilts. Prepubertal gilts (n = 18) were assigned to donor or recipient groups and donors were allocated to TN or HS environments. Blood was collected from HS donors and TN donors exposed to 24-hours of HS or TN conditions, respectively. Serum was infused into recipients housed in TN conditions via indwelling jugular catheters. Over a 24-hour period approximately 20% of the estimated recipient gilt serum volume from donors (pooled by treatment) was infused into recipients. After infusions were completed, gilts were euthanized and tissues collected. Increased rectal temperatures were observed in HS recipients compared to TN recipients (P ≤ 0.05). Protein extracts from liver and ovary underwent proteomic analysis via liquid-chromatography with tandem mass-spectrometry (LC-MS/MS) to assess protein abundance. In the liver and ovary, we identified 135 and 264 proteins, respectively, that were differentially abundant between TN and HS recipients (P < 0.10). Gene Ontology enrichment analysis identified alterations to pathways involved in hormone regulation, immune response, and apoptosis. Collectively, these data demonstrate gilts receiving HS serum experienced altered endocrine and metabolic function compared to gilts receiving TN serum. This project was supported in part by the Iowa Pork Producers Association. USDA is an equal opportunity provider and employer. [ABSTRACT FROM AUTHOR]

Zearalenone (ZEA) is an estrogenic mycotoxin produced by strains of Fusarium and is often inadvertently consumed via feed contamination. Heat stress (HS) occurs when heat accumulation exceeds heat dissipation resulting in increased body temperature. Independently, HS and ZEA cause swine reproductive dysfunction such as delayed puberty onset, altered circulating steroid hormones and irregular estrous cycles. During HS, gilts become hyperinsulinemic and insulin regulates hepatic and ovarian chemical metabolism. We hypothesized that during HS, ZEA-induced alterations to reproductive parameters are heightened such that HS is additive to ZEA-induced reproductive toxicity. Prepubertal crossbred gilts (n = 38) were randomly assigned to six treatment groups: thermal neutral (TN) ad libitum fed controls (TNCT; n = 6); TN + ZEA (2 ppm; TNZ; n = 6); pair-fed (PF) control (PFCT; n = 6); PF + ZEA (2 ppm; PFZ; n = 6); cyclical HS control (HSCT; n = 7); and HS + ZEA (2 ppm; HSZ; n = 7) for 7 d. Ovarian and uterine weights (g) were measured, and nipple and vulva diameters (l × w; mm2) were assessed by digital calipers. Ovarian weight was decreased (P = 0.04) in the PFZ relative to PFCT, but ZEA did not affect ovarian weight in the other groups (P > 0.73). There was no impact of ZEA exposure on uterine weight (P > 0.22) or nipple diameter (P > 0.51) in any treatment groups, respectively. There was no effect of ZEA on vulva size in either of the TN groups; however, vulva diameter increased (P = 0.04) in the HSZ relative to HSCT. These data suggest that HS exaggerates some ZEA-induced phenotypic effects in prepubertal gilts. This project was supported by the Iowa Pork Producers Association. [ABSTRACT FROM AUTHOR]

Heat stress represents one of the costliest issues in animal agriculture as it compromises a variety of production parameters including growth and reproduction. When animals are exposed to heat stress, physiological and metabolic changes are needed to cope with the heat insult to maintain euthermia. The most well-established adaptation across species involves a marked reduction in feed intake. Additionally, heat-stressed animals alter their carbohydrate, lipid, and protein metabolism; a mechanism characterized by a paradoxical increase in circulating insulin. This altered nutrient partitioning appears to be mediated by the effects of heat stress on gastrointestinal health. Heat-stressed animals redistribute blood flow from the splanchnic bed to the periphery in a coordinated attempt to maximize heat dissipation. This circulatory adaptation reduces blood and nutrient delivery to the gastrointestinal tract which compromises intestinal infrastructure barrier. Consequently, a dysfunctional intestinal barrier allows for the translocation of dietary and microbial (i.e., lipopolysaccharide [LPS], from Gram negative bacteria) antigens from the lumen to the basolateral membrane, stimulating a local and systemic inflammatory response. Interestingly, there are remarkable metabolic and physiological similarities between animals suffering from heat stress and severe endotoxemia; in both conditions, there is an increase in circulating insulin despite marked reductions in feed intake, a scenario energetically difficult to explain. The likelihood that LPS is an insulin secretagogue explains the hyperinsulinemia we and others observe in a variety of heat stress models. Inflammation induced by LPS elicits the production of pro-inflammatory cytokines. When activated, the immune system utilizes a considerable amount of energy (glucose), which redirects nutrients away from production purposes (i.e., growth, reproduction); thus, negatively compromising animal production efficiency. Therefore, identifying strategies designed to minimize intestinal permeability, improve the immune response, and enhance animal productivity during a thermal load is of particular interest. Nutritional interventions are practical and cost-effective approaches to mitigate the detrimental effects of heat stress on animal health and productivity and to minimize agricultural economic losses. [ABSTRACT FROM AUTHOR]

Objectives were to determine the effects of mitoquinol (MitoQ) on performance, metabolism, and inflammation during acute heat stress (HS) in growing pigs. Crossbred barrows (n=32; 59±1 kg BW) where blocked by BW and randomly assigned to 1 of 4 therapeuticenvironmental treatments: 1) thermoneutral (TN) control (n=8; TNCtl), 2) TN and MitoQ (n=8; TNMitoQ), 3) HS control (n=8; HSCtl), or 4) HS and MitoQ (n=8; HSMitoQ). The trial consisted of two experimental periods (P). During P1 (2d), pigs were fed ad libitum and housed in TN conditions (20.6±0.1°C). During P2 (24h), HSCtl and HSMitoQ pigs were exposed to continuous HS (35.2±0.03°C); while TNCtl and TNMitoQ remained in TN conditions. Mitoquinol was orally administered twice daily (0700 and 1800 h; 40 mg/d) during P1 and P2. Pigs exposed to HS had increased rectal temperature, skin temperature, and respiration rate (1.46°C, 6.79°C, and 101 bpm, respectively; P< 0.01) compared to their TN counterparts. Acute HS markedly decreased feed intake (67%; P< 0.01). Additionally, HS pigs lost BW compared to their TN counterparts (-4.7 vs. +1.6 kg, respectively; P< 0.01); however, the reduction in BW was less severe in HSMitoQ compared to HSCtl pigs (-3.85 vs. -5.50 kg, respectively; P< 0.01). Circulating glucose increased in HSMitoQ relative to HSCtl pigs (15%; P=0.04). Nonesterified fatty acid (NEFA) concentrations were increased in HS compared to TN pigs (P< 0.01), although this difference was influenced by increased NEFA in HSCtl relative to HSMitoQ pigs (251 vs. 142 µEq/L; P< 0.01). Insulin:feed intake tended to increase in HS relative to TN pigs (P=0.09). Overall, no differences in blood urea nitrogen or cell blood counts were observed across treatments (P >0.10). In conclusion, acute HS exposure negatively altered animal performance and metabolism; however, administering MitoQ appeared to ameliorate the HS response. [ABSTRACT FROM AUTHOR]

Objectives were to determine the effects of rapamycin on biomarkers of metabolism and inflammation during acute heat stress (HS) in growing pigs. Crossbred barrows (n=32; 63.5±0.8 BW) where blocked by BW and randomly assigned to 1 of 4 therapeutic-environmental treatments: 1) thermoneutral (TN) control (n=8; TNCtl), 2) TN and rapamycin (n=8; TNRapa), 3) HS control (n=8; HSCtl), or 4) HS and rapamycin (n=8; HSRapa). The trial consisted of 2 experimental periods (P). During P1 (10d), pigs were fed ad libitum and housed in TN conditions (21.3±0.01°C). During P2 (24h), HSCtl and HSRapa pigs were exposed to constant HS (35.5±0.1°C); while TNCtl and TNRapa remained in TN conditions. Rapamycin (0.15 mg/kg BW) was orally administered twice daily (0700 and 1800 h) during P1 and P2. HS increased rectal temperature, skin temperature, and respiration rate compared to TN counterparts (1.28°C, 8.68°C, and 87 bpm, respectively; P< 0.01). Feed intake (FI) markedly decreased in HS relative to TN treatments (64%; P< 0.01). Additionally, pigs exposed to HS lost BW (4 kg; P< 0.01), while TN pigs gained BW (0.7 kg; P< 0.01). Overall, circulating white blood cells decreased in HS compared to TN pigs (19%; P=0.01). Circulating neutrophils did not differ across treatments; however, lymphocytes, monocytes, and basophils decreased in HS relative to TN pigs (23, 33, and 38%, respectively; P=0.07). Despite marked changes in phenotypic parameters, circulating glucose and blood urea nitrogen did not differ among treatments (P >0.10). However, insulin:FI increased in HS relative to TN treatments (P=0.04). Plasma nonesterified fatty acids (NEFA) increased in HS relative to TN treatments; although this difference was driven by increased NEFA in HSCtl compared to TN and HSRapa pigs (P< 0.01). In summary, pigs exposed to HS had altered phenotypic, metabolic, and leukocyte responses; however, rapamycin administration had little to no effect on any of the variables measured. [ABSTRACT FROM AUTHOR]