Disease relevance of UC

• These results also suggest that reducing placental and fetal weights will likely result in increased uterine capacity [1].
• Recent evidence indicates that one critical component of the uterine capacity in pigs is placental efficiency, or the body weight of a piglet divided by the mass of its placenta [2].
• The incompatibility between increased numbers of conceptuses surviving to the postimplantation period, in the absence of increased uterine capacity, offers a biological explanation for increased variability in birth weight and postnatal growth performance reported in greater parity sows [3].
• Knowledge of the basic mechanisms regulating uterine development is expected to suggest means to increase uterine capacity, litter size, and neonatal survival, as well as ameliorate certain types of infertility [4].

High impact information on UC

• Early progesterone treatment reduced (P < 0.05) litter size (a measure of uterine capacity in UHO gilts) [5].
• In contrast to the effect of progesterone treatment, mifepristone decreased uterine capacity by decreasing the number of small conceptuses [5].
• Litter size in the pig is limited by uterine capacity, which is dependent on uterine size, placental size, and vascularity [6].
• Strategic manipulation of these physiological mechanisms may offer therapeutic schemes to improve uterine capacity, conceptus survival, and reproductive health of domestic animals and humans [7].
• Effect of progesterone, mifepristone, and estrogen treatment during early pregnancy on conceptus development and uterine capacity in Swine [5].

Biological context of UC

• Two regions possessed suggestive evidence for QTL affecting AP on chromosomes 1 and 10, and one suggestive region on chromosome 8 was identified for UC [8].
• A multigeneration crossbred Meishan-White composite resource population was used to identify quantitative trait loci (QTL) for age at first estrus (AP) and the components of litter size: ovulation rate (OR; number of ova released in an estrous period) and uterine capacity (UC) [8].
• These results indicate that the EPOR SNP is associated with UC and litter size in two distinct populations and could be useful in increasing litter size in swine that are not limited in OR [9].
• These results indicate that selection for ovulation rate decreased total fetal and fetal heart weights, and that selection for UC altered the relationship between total fetal and fetal liver weights during early gestation [10].
• White crossbred gilts from a randomly selected control line, a line selected for ovulation rate, and a line selected for uterine capacity (UC) were unilaterally hysterectomized-ovariectomized at 160 d of age, mated at estrus, and slaughtered at 45, 65, 85, and 105 d of gestation (9 to 18 gilts for each line x day combination) [10].

Anatomical context of UC

• Potentially viable embryos then could be further reduced to uterine capacity, the maximum number of fetuses that a female can carry to term [11].
• This response was due to an increase of 1.30 +/- .54 eggs in ovulation rate (measured by the number of corpora lutea in cyclic and pregnant gilts) and .66 +/- 1.28 pigs in uterine capacity (measured after unilateral hysterectomy-ovariectomy) [12].
• Compared with Western breeds of swine, ME females reach puberty earlier, ovulate more ova per estrus, and have greater uterine capacity, while intact males (boars) have smaller testes and extremely elevated plasma levels of pituitary-derived glycoprotein hormones [13].
• Both early embryonic survival (factors inherent to the ovum and uterus, which occur before day 25 of gestation) and uterine capacity (factors inherent to uterine limitation, which occur from 30 days of gestation to parturition) may contribute to prenatal survival [14].

Associations of UC with chemical compounds

• A series of experiments was performed to investigate the influence of progesterone at Days 2 and 3 of pregnancy on conceptus development and uterine capacity [5].
• The effect of prepubertal retinyl palmitate treatment on uterine development and uterine capacity was determined [15].
• Effect of estrone treatment from day 30 to 45 of pregnancy on endometrial protein secretion and uterine capacity [16].
• Uterine capacity and progestin levels in superinducted gilts [17].

Other interactions of UC

• Linkage mapping of a SNP in the porcine MADH1 gene to a region of chromosome 8 that contains QTL for uterine capacity [18].
• The epidermal growth factor (EGF) gene, on porcine chromosome 8, may influence uterine capacity because of its growth-promoting activities [19].
• Allelic variation in the secreted folate binding protein gene is associated with uterine capacity in swine [20].

Analytical, diagnostic and therapeutic context of UC

• Previous gene mapping analyses revealed a quantitative trait locus for uterine capacity on chromosome 8 [21].
• In Exp. 3, uterine growth and ovarian compensation after unilateral ovariectomy and hysterectomy at 60 d of age were determined in 85 crossbred gilts from 60 to 180 d of age to evaluate the unilateral ovariohysterectomy model for studying association of uterine length before puberty and subsequent uterine capacity [22].
• The aim of this study was to determine whether there is any association between the prenatal survival rate and placental size at 70 days of gestation, the vaginal length [catheter penetration length during artificial insemination (AI)] and the uterine capacity in a homogeneous group of gilts [23].

References