scholarly journals Heat stress during the luteal phase decreases luteal size but does not affect circulating progesterone in gilts1

2019 ◽  
Vol 97 (10) ◽  
pp. 4314-4322 ◽  
Author(s):  
Katie L Bidne ◽  
Matthew R Romoser ◽  
Jason W Ross ◽  
Lance H Baumgard ◽  
Aileen F Keating

Abstract Heat stress (HS) occurs when heat dissipation mechanisms are insufficient to maintain euthermia, and it is associated with seasonal infertility (SI), which manifests as smaller litters, longer wean-to-estrus interval, increased abortions, and reduced conception rates. To understand HS-induced mechanisms underlying SI, crossbred post-pubertal gilts (167 ± 10 kg; n = 14) experienced either thermal neutral (TN, 20 ± 1 °C, n = 7) or cyclical HS (35 ± 1 °C for 12 h and 31.6 °C for 12 h, n = 7) conditions from 2 to 12 d post-estrus (dpe). Estrous cycles were synchronized via altrenogest administration for 14 d, phenotypic manifestation of estrus was observed and gilts were assigned to experimental treatment. Gilts were limit fed 2.7 kg daily with ad libitum water access. Blood was collected at 0, 4, 8, and 12 dpe via jugular venipuncture and animals were humanely euthanized at 12 dpe. The corpora lutea (CL) width were measured via digital calipers on both ovaries, and CL from one ovary were excised, weighed, and protein and steroid abundance analyzed via western blotting and ELISA, respectively. Relative to TN, HS increased (P < 0.01) rectal temperature and respiration rates and reduced (P < 0.01) feed intake. The CL from HS ovaries were reduced in diameter (P < 0.05) and weight (P < 0.01) relative to those from TN animals. No difference (P = 0.38) in CL or serum progesterone concentrations between groups was observed at any time point, though at 12 dpe the serum progesterone:CL weight was increased (P < 0.10) by HS. No treatment differences (P = 0.84) in circulating insulin were observed. Luteal protein abundance of steroid acute regulatory protein, 3 beta-hydroxysteroid, or prostaglandin F2α receptor were not different between treatments (P = 0.73). Taken together, these data demonstrate that the CL mass is HS sensitive, but this phenotype does not appear to be explained by the metrics evaluated herein. Regardless, HS-induced decreased CL size may have important implications to pig SI and warrants additional attention.

2020 ◽  
Vol 26 (8) ◽  
pp. 585-600
Author(s):  
Natalia Pascuali ◽  
Leopoldina Scotti ◽  
Gonzalo Oubiña ◽  
Ignacio de Zúñiga ◽  
Mariana Gomez Peña ◽  
...  

Abstract Although advances in the prediction and management of ovarian hyperstimulation syndrome (OHSS) have been introduced, complete prevention is not yet possible. Previously, we and other authors have shown that vascular endothelial growth factor, angiopoietins (ANGPTs) and sphingosine-1-phosphate are involved in OHSS etiology. In addition, we have demonstrated that ovarian protein levels of platelet-derived growth factor (PDGF) ligands -B and -D decrease in an OHSS rat model, whilst PDGFR-β and ANGPT2 remain unchanged. In the present work, we investigated the role of PDGF-B in OHSS by evaluating ligand protein levels in follicular fluid (FF) from women at risk of developing OHSS and by using an immature rat model of OHSS. We demonstrated that PDGF-B and PDGF-D are lower in FF from women at risk of developing OHSS compared to control patients (P &lt; 0.05). In the OHSS rat model, PDGF-B (0.5 µg/ovary) administration decreased ovarian weight (P &lt; 0.05), reduced serum progesterone (P &lt; 0.05) and lowered the percentage of cysts (P &lt; 0.05), compared to untreated OHSS rats, but had no effect on the proportion of follicles or corpora lutea (CL). PDGF-B treatment also restored the expression of steroidogenic acute regulatory protein (P &lt; 0.05) and P450 cholesterol side-chain cleavage enzyme (P &lt; 0.01) to control levels. In addition, PDGF-B increased the peri-endothelial cell area in CL and cystic structures, and reduced vascular permeability compared to untreated OHSS ovaries. Lastly, PDGF-B increased the levels of junction proteins claudin-5 (P &lt; 0.05), occludin (P &lt; 0.05) and β-catenin (P &lt; 0.05), while boosting the extracellular deposition of collagen IV surrounding the ovarian vasculature (PP &lt; 0.01), compared to OHSS alone. In conclusion, our findings indicate that PDGF-B could be another crucial mediator in the onset and development of OHSS, which may lead to the development of novel prediction markers and therapeutic strategies.


2020 ◽  
Vol 98 (Supplement_3) ◽  
pp. 214-214
Author(s):  
Crystal M Roach ◽  
Edith J Mayorga ◽  
Jason W Ross ◽  
Lance H Baumgard ◽  
Aileen F Keating

Abstract 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 &gt; 0.73). There was no impact of ZEA exposure on uterine weight (P &gt; 0.22) or nipple diameter (P &gt; 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.


2013 ◽  
Vol 25 (1) ◽  
pp. 303
Author(s):  
M. Taniguchi ◽  
E. Sasaki ◽  
T. Otoi

Rapid oestrous induction after embryo collection shortens the calving interval of donor cows and improves the efficiency of embryo production. This study aimed to evaluate whether large nonovulated follicles present at the time of embryo collection affect oestrous induction after embryo collection in Japanese Black donor cows. Superovulation treatments were initiated during mid-cycle (9–12 days after oestrus) with 20 AU of FSH (Antrin; Kyoritsu Seiyaku Corp., Tokyo, Japan) administered intramuscularly through 6 injections of decreasing doses at 12-h intervals. On the third day, the cows received 0.5 mg of prostaglandin F2α (PGF; Resipron-C, Asuka Seiyaku Corp., Tokyo, Japan) to induce regression of the corpus luteum and were artificially inseminated 60 to 72 h later. Embryos were collected 7 days after AI. All cows received 0.5 mg of PGF immediately after embryo collection and were allocated to 1 of 2 groups: cows (n = 6) with one or more large nonovulated follicles >18 mm in diameter (Group 1) and cows (n = 5) with no large follicles (Group 2). Oestrus detection was performed by visual observation conducted twice daily after embryo collection. Ovarian ultrasonographic examinations and blood collections (for serum progesterone [P4] and oestradiol [E2] measurements) were performed once daily until the next ovulation. Statistical significance was determined using Student’s t-test. There were no differences in the numbers of corpora lutea, ova/embryos, and transferable embryos or the percentages of transferable embryos between the 2 groups. The interval (mean ± SEM) from embryo collection to the appearance of the dominant follicle and to ovulation was longer (P < 0.05) in Group 1 (5.3 ± 0.7 and 11.0 ± 1.0 days, respectively) than in Group 2 (2.6 ± 0.7 and 8.2 ± 0.7 days, respectively). However, the interval from embryo collection to luteolysis (P4 <1 ng mL–1) did not differ between the 2 groups (4.0 ± 0.7 v. 3.6 ± 0.7 days). In conclusion, the presence of large nonovulated follicles at the time of embryo collection may delay oestrous induction after embryo collection.


Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1879-1885 ◽  
Author(s):  
Christine K. Ratajczak ◽  
Katie L. Boehle ◽  
Louis J. Muglia

Evidence in humans and rodents suggests that normal circadian rhythmicity is important for supporting reproductive function. A molecular clock underlies circadian rhythmicity. Impaired fertility is observed in some genetically altered mice with deficiencies in genes of the molecular clock, suggesting a critical role for these genes in reproduction. Here we systematically characterize the reproductive phenotype of females deficient in the clock gene Bmal1. Bmal1−/− females are infertile. They exhibit progression through the estrous cycle, although these cycles are prolonged. Normal follicular development occurs in Bmal1−/− females, and healthy embryos of the expected developmental stage are found in the reproductive tract of Bmal1−/− females 3.5 d after mating to wild-type males. However, serum progesterone levels are significantly lower in Bmal1−/−vs. Bmal1+/± females on d 3.5 of gestation. Low progesterone levels in Bmal1−/− females are accompanied by decreased expression of steroidogenic acute regulatory protein in corpora lutea of Bmal1−/−vs. Bmal1+/± females. Whereas implantation of embryos is not observed in untreated or vehicle-treated Bmal1−/− females, exogenous administration of progesterone to Bmal1−/− females is able to reinstitute implantation. These data suggest that implantation failure due to impaired steroidogenesis causes infertility of Bmal1−/− females.


2019 ◽  
Vol 97 (12) ◽  
pp. 4965-4973 ◽  
Author(s):  
Jacob T Seibert ◽  
Malavika K Adur ◽  
Ronald B Schultz ◽  
Porsha Q Thomas ◽  
Zoe E Kiefer ◽  
...  

Abstract Heat stress (HS) negatively affects both human and farm-animal health and undermines efficiency in a variety of economically important agricultural variables, including reproduction. HS impairs the intestinal barrier, allowing for translocation of the resident microflora and endotoxins, such as lipopolysaccharide (LPS), from the gastrointestinal lumen into systemic circulation. While much is known about the cellular function of heat shock proteins (HSPs) in most tissues, the in vivo ovarian HSP response to stressful stimuli remains ill-defined. The purpose of this study was to compare the effects of HS or LPS on ovarian HSP expression in pigs. We hypothesized that ovarian HSPs are responsive to both HS and LPS. Altrenogest (15 mg/d) was administered per os for estrus synchronization (14 d) prior to treatment and three animal paradigms were used: (i) gilts were exposed to cyclical HS (31 ± 1.4 °C) or thermoneutral (TN; 20 ± 0.5 °C) conditions immediately following altrenogest withdrawal for 5 d during follicular development; (ii) gilts were subjected to repeated (4×/d) saline (CON) or LPS (0.1 μg/kg BW) i.v. infusion immediately following altrenogest withdrawal for 5 d; and (iii) gilts were subjected to TN (20 ± 1 °C) or cyclical HS (31 to 35 °C) conditions 2 d post estrus (dpe) until 12 dpe during the luteal phase. While no differences were detected for transcript abundances of the assessed ovarian HSP, the protein abundance of specific HSP was influenced by stressors during the follicular and luteal phases. HS during the follicular phase tended (P &lt; 0.1) to increase ovarian protein abundance of HSP90AA1 and HSPA1A, and increased (P ≤ 0.05) HSF1, HSPD1, and HSPB1 compared with TN controls, while HS decreased HSP90AB1 (P = 0.01). Exposure to LPS increased (P &lt; 0.05) HSP90AA1 and HSPA1A and tended (P &lt; 0.1) to increase HSF1 and HSPB1 compared with CON gilts, while HSP90AB1 and HSPD1 were not affected by LPS. HS during the luteal phase increased (P &lt; 0.05) abundance of HSPB1 in corpora lutea (CL), decreased (P &lt; 0.05) CL HSP90AB1, but did not impact HSF1, HSPD1, HSP90AA1, or HSPA1A abundance. Thus, these data support that HS and LPS similarly regulate expression of specific ovarian HSP, which suggest that HS effects on the ovary are in part mediated by LPS.


2002 ◽  
Vol 283 (6) ◽  
pp. E1308-E1315 ◽  
Author(s):  
Kazuhiro Minegishi ◽  
Mamoru Tanaka ◽  
Osamu Nishimura ◽  
Shinji Tanigaki ◽  
Kei Miyakoshi ◽  
...  

We investigated the contribution of neutrophils to prostaglandin (PG)F2α-induced luteolysis and the role of reactive oxygen species (ROS) as potential mediators of neutrophil accumulation in regressing corpora lutea of superovulated rats. On day 8of pseudopregnancy, subcutaneous injection of PGF2α(500 μg) significantly increased rhodamine 6G-labeled leukocyte adhesion in luteal venules, as observed by intravital microscopy. Neutrophil accumulation was confirmed by significantly increased myeloperoxidase (MPO) activity. Pretreatment with anti-leukocyte antibody (CD18-directed monoclonal antibody, WT-3) significantly inhibited the PGF2α-induced increases in adherent leukocytes and MPO activity. Anti-leukocyte antibody also maintained serum progesterone concentrations. Pretreatment with oxygen free radical scavengers, superoxide dismutase (50,000 U/kg) and catalase (90,000 U/kg), also attenuated these PGF2α-induced alterations. Corpora lutea preloaded with dichlorodihydrofluorescein diacetate succinimidyl ester, a fluorescent indicator for determining intracellular ROS generation, exhibited an increase in fluorescence after PGF2αtreatment. These findings suggest that leukocyte-endothelium interactions mediated by ROS generation are important in PGF2α-induced luteolysis in rats.


1977 ◽  
Vol 57 (1) ◽  
pp. 47-51 ◽  
Author(s):  
J. G. MANNS ◽  
M. S. WENKOFF ◽  
W. M. ADAMS ◽  
G. RICHARDSON

Two injections of prostaglandin F2α (PGF2α) spaced 12 days apart were used to synchronize estrus in Hereford heifers. Animals were inseminated at 75 h (group 2), 80 h (group 3) or 85 h (group 4) after the second injection of PGF2α. Untreated control animals (group 1) were inseminated as detected in estrus over an observation period of approximately 35 days. Immediately before, and 24 h after each PGF2α injection, blood was collected for progesterone assay. Fertility expressed as calving rates was as follows: group 1, 33/77 (43%); group 2, 30/79 (38%); group 3, 29/79 (37%); group 4, 20/73 (27%). Fertility was depressed at 85 h vs. control (P < 0.05) in PGF2α-treated animals but there were no other significant differences. Progesterone assays showed that 65% of animals had progesterone-secreting corpora lutea at the first injection of PGF2α. There was no relationship between fertility and either serum progesterone concentration or the day of the cycle at the second injection of PGF2α.


2021 ◽  
Vol 99 (Supplement_1) ◽  
pp. 107-108
Author(s):  
Crystal M Roach ◽  
Edith J Mayorga ◽  
Lance H Baumgard ◽  
Jason W Ross ◽  
Aileen F Keating

Abstract 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 &lt; 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 &lt; 0.05). During HS, ZEA differentially affected (P &lt; 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.


Sign in / Sign up

Export Citation Format

Share Document