title: Ovulation rate, embryo mortality and intrauterine growth retardation in obese swine with gene polymorphisms for leptin and melanocortin receptors.
abstract: The Mediterranean Iberian pigs are obese genotypes, due to a leptin resistance syndrome related to leptin receptor gene polymorphisms. The Iberian pig is affected by a lower prolificacy when compared to lean breeds, and thus may constitute a good animal model for adverse effects of obesity in reproductive performance. The present study determined possible differences in rates of ovulation and embryo implantation and later incidence of embryo mortality and intrauterine growth retardation (IUGR) in sows of Iberian breed (n = 23) and highly-prolific lean commercial crosses (Large White × Landrace, n = 17) at two critical periods of swine pregnancy: Day 21 (just after achievement of trophoblast attachment) and Day 35 (just after completion of the transition from late embryo to early foetal stage). Two different reproductive performances were identified in the Iberian breed; 58.3% of the females had lower ovulation rates than LWxL (13.2 ± 2.3 vs 22.5 ± 1.6, P < 0.05), but 41.7% had a similar number of ovulations (18.2 ± 3.9). However, those Iberian sows having high ovulatory rates showed a high incidence of regression of corpora lutea and embryo losses between Days 21 and 35, which was not found in Iberian females with low ovulation rates; therefore, the number of viable embryos was similar in both Iberian groups (8.2 ± 1.0 and 8.4 ± 1.0) and lower that in highly-prolific LWxL (14.8 ± 1.8, P < 0.05). At Day 35, a total of 167 conceptuses (73 LWxL and 94 IB) were evaluated for IUGR. The LWxL conceptuses were longer and wider than Iberian (69.5 ± 0.1 and 64.4 ± 0.1 vs 49.9 ± 0.1 and 41.9 ± 0.1 mm, P < 0.0001). However, Iberian conceptuses were heavier than LWxL (107.4 ± 6.6 vs 68.6 ± 2.4 g) due to a lower quantity of fluids and a higher development of the placental tissues in comparison to the embryo itself. In conclusion, current study indicates a bimodal effect of obese genotypes on reproductive performances, either by lowering ovulation rate or by increased embryo losses in the first third of pregnancy.
authors.affiliation: NUTEGA, Madrid, Spain.
authors.forename: P
authors.initials: P
authors.lastname: Gonzalez-Añover
authors.forename: T
authors.initials: T
authors.lastname: Encinas
authors.forename: L
authors.initials: L
authors.lastname: Torres-Rovira
authors.forename: P
authors.initials: P
authors.lastname: Pallares
authors.forename: J
authors.initials: J
authors.lastname: Muñoz-Frutos
authors.forename: E
authors.initials: E
authors.lastname: Gomez-Izquierdo
authors.forename: R
authors.initials: R
authors.lastname: Sanchez-Sanchez
authors.forename: A
authors.initials: A
authors.lastname: Gonzalez-Bulnes
mesh_terms: D000818:Animals; D010064:Embryo Implantation; D020964:Embryo Loss / Q000235:genetics; D047108:Embryonic Development; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology* / Q000235:genetics; D009765:Obesity / Q000150:complications* / Q000235:genetics; D009929:Organ Size; D010060:Ovulation / Q000502:physiology*; D011110:Polymorphism, Genetic; D011247:Pregnancy; D054411:Receptors, Leptin / Q000235:genetics*; D044101:Receptors, Melanocortin / Q000235:genetics*; D034421:Sus scrofa; D014599:Uterus / Q000033:anatomy & histology
chemical_list: D054411:Receptors, Leptin; D044101:Receptors, Melanocortin