Location:2009 Annual Report
1a. Objectives (from AD-416)
Objective 1: Identify adipose tissue genes and physiological pathways underlying variation in seasonal infertility in swine. Sub-objective 1.A: Identify physiological pathways that underlie the relationship between reproductive losses due to seasonal infertility. Sub-objective 1.B: Identify changes in adipose tissue gene expression underlying variation in seasonal infertility in swine. Objective 2: Define physiological factors contributing to gastrointestinal-microbial population and immune function that are associated with seasonal infertility in sows. Sub-objective 2.A: Identify microbial popoulation changes and sensitivity to antimicrobials associated with seasonal infertility. Sub-objective 2.B: Characterize functional changes in systemic and tissue level inflammatory and immune cells that are associated with seasonal infertility in the sow. Objective 3: Determine if a relationship exists between reproductive losses due to seasonal infertility and adipocyte function, metabolism and uterine function. Sub-objective 3.A: Identify genes that are related to physiological pathways that are associated with seasonal infertility and associated adipocyte function and metabolism. Sub-objective 3.B: Identify genes that are related to physiological pathways that are associated with seasonal infertility and pregnancy failure. Objective 4: To map patterns of gene expression that underlie adipose tissue deposition and identify intervention control points to reduce fat deposition.
1b. Approach (from AD-416)
Seasonal infertility is proposed to be due to many stressors such as social environment, management, nutrition, thermal environment, and photoperiod. These factors affect neuroendocrine function of the sow, resulting in reduced fertility. It is well established that level of nutrition during lactation affects body condition and weaning-to-estrus interval. A manifestation of these stressors is an alteration in metabolic mass, a reduction in food intake and its correlated metabolic rate, which may be the triggering mechanism. Thus, seasonal infertility may also in part be due to reduced body fat and altered adipocyte function and secretion of regulatory proteins. An integrated and multidisciplinary approach, combining microarray technology with the study of endocrinology, adipocyte function, immune function and gastrointestinal microbial ecology in order to elucidate the mechanisms that contribute to seasonal infertility in the sow. This systems approach will provide an unprecedented opportunity to identify important genes and gene interactions and physiological pathways contributing to variation in seasonal fertility.
3. Progress Report
Data, adipose tissue, blood samples, and fecal samples were collected from four groups of multiparous sow farrowing in the winter (December-March) and in the summer (June-September). Blood and fecal samples were analyzed. Based on retrospective classification criteria used to classify sows as seasonally infertile, there was no difference between winter and summer farrowing sows. Therefore, adipose tissue was not subjective to microarray analysis.
1. Identify microbial popoulation changes and sensitivity to antimicrobials associated with seasonal infertility. Serotyping and antimicrobial susceptibility tests were conducted on fecal samples collected from sows farrowing in the winter and summer. There were no seasonal differences detected in gut microbial population or sensitivity to antimicrobials.
2. Characterize functional changes in systemic and tissue level inflammatory and immune cells that are associated with seasonal infertility in the sow. Winter sows had a lower level of basal neutrophil and mononuclear cell inflammatory activation than the summer sows. Summer sows also exhibited a decline in circulating IgG levels which is consistent with the change in neutrophil and mononuclear cell inflammatory responses observed. These results indicate seasonal related suppression of adaptive immune function in the sow.
Barb, C.R., Hausman, G.J. 2009. Insulin-like growth factor-I feedback regulation of growth hormone and luteinizing hormone secretion in the pig: Evidence for a pituitary site of action. Animal. v.3(6) p. 844-849.