Heat stress (HS) is a major economic strain for the US swine industry. In terms of reproduction, seasonal infertility is associated with HS, characterized by lengthened wean-to-estrus interval (WEI), increased spontaneous abortions and increased number of rebreeds. Unfortunately, there is unlikely to be a reduction in the strain that HS imparts to the swine industry and the negative effects of HS are likely to become more severe if climate change continues as some predict and most models forecast more extreme summer conditions in US pig-producing areas. Also, genetic selection for rapid muscle growth is thought to increase pig sensitivity to HS as these animals have a higher basal metabolic rate (i.e. greater heat load). The biological explanation for seasonal infertility is poorly understood, and until such time that a thorough understanding is gained, development of mitigating strategies will remain limited. We have discovered that heat-stressed pigs have both increased circulating insulin and lipopolysaccharide (LPS) levels. We believe that higher systemic insulin and LPS detrimentally influence ovarian biological, thereby hampering reproduction. Our central hypothesis is that heat-induced elevated insulin and lipopolysaccharide (LPS) are causative factors in seasonal infertility. We had two objectives in this project: 1) To investigate ovarian impacts of hyperinsulinemia and 2) Determine effects of increased circulating LPS on ovarian function.
Prior to this proposal, we had discovered that HS altered a number of molecular pathways in the ovary, and these alterations could all adversely impact ovarian function as well as pregnancy maintenance. We published these data in the journal Biology of Reproduction, a premiere journal in reproductive biology. However, we did not know the causative agents. Through the current work, we have discovered the following: 1) HS in the presence of an insulin bolus 15 prior to tissue collection resulted in altered levels of genes and proteins in the pathway through which ovarian hormones are generated, thus, we have additional evidence that HS alters ovarian hormones which could be responsible for lengthened WEI in swine during summer months. 2) Both HS and LPS increased a pathway that is involved in regulating both the health of the ovulated oocyte as well as ovarian hormone production. 3) Acute LPS induced a response in the ovary a mere 8 h after the exposure. 4) LPS altered the machinery responsible for generation of ovarian hormones in a manner that had similarities as well as differences with HS alone. Because we had technical difficulties in counting follicles within the ovary, we extended the study to examine if there could be additional “turnover” of the chief ovarian hormone, 17β-estradiol, within the ovary during HS. We discovered this to be true, the machinery responsible for degrading 17β-estradiol in a cyclical fashion is altered by HS, indicating that this could also play a role in seasonal infertility in swine. Identification of these HS- as well as LPS-induced ovarian changes have set the stage to continue our investigations to lead to mitigation interventions to minimize seasonal infertility in swine.
Producer Take Home messages:
• HS and LPS alter a pathway in the ovary that regulates when oocyte (egg)-containing follicles are activated to grow and ovulate.
• HS and LPS affect the mechanisms by which the ovary produces key female hormones required for ovulation and maintenance of pregnancy.
• The ovarian transporter protein responsible for degrading 17β-estradiol (estrogen) in a cyclical pattern during the estrous cycle is altered by HS.
Contact Information Aileen F. Keating, 2356J Kildee Hall, Department of Animal Science, Iowa State University; Telephone 515-294-3849; email [email protected]