Litter size and piglet traits of gilts with different prolactin receptor genotypes.

Seventy-seven Large White x Meishan F2 crossbred gilts with prolactin receptor (PRLR) genotype AA (n = 26), AB (n = 36) and BB (n = 15) were compared for teat number (FTm), age at first estrus, gestation length (GL), litter size, and litter means of functional teat number (FTp), birthweight (BW), and pre-weaning growth rate (GR). Own placental information was available for 88% of 620 live-born piglets (62 gilts), since placentae were labeled during farrowing. The effect of PRLR genotype of the mother on average placenta weight (PLW) and placenta efficiency (EFF = BW/PLW), was therefore, also analyzed, PRLR genotype significantly (P < 0.05) affected age at first estrus and, as a result (since the gilts were inseminated at a fixed estrus number), age and bodyweight at insemination. Furthermore, PRLR genotype affected total number of piglets born (TNB, P = 0.056) and number of piglets born alive (NBA, P = 0.072), but it did not affect (P > 0.3) GL, BW or GR, neither before nor after correction for litter size. BB gilts were significantly younger at first estrus and younger and lighter at insemination than AA gilts (P < 0.05). AA gilts had larger TNB (P = 0.047) and tended to have a larger NBA (P = 0.062) than BB gilts. TNB was 11.4 +/- 0.7, 10.8 +/- 0.6, and 8.8 +/- 0.9; NBA was 11.1 +/- 0.6, 10.5 +/- 0.6, and 8.7 +/- 0.9; BW was 1309 +/- 40, 1277 +/- 34, and 1290 +/- 53 g; and GL was 113.6 +/- 0.3, 113.8 +/- 0.3, and 113.5 +/- 0.4 days for AA, AB and BB gilts, respectively. The effects on litter size and age at first estrus are independent effects. PRLR affected PLW (P = 0.050) and EFF (P = 0.066), resulting in a difference between AA and BB gilts. PLW was 160 +/- 9, 181 +/- 7 and 196 +/- 11 g and EFF was 7.6 +/- 0.2, 7.3 +/- 0.2 and 6.7 +/- 0.3 for AA (n = 19), AB (n = 29) and BB (n = 14) gilts, respectively. After correction for TNB, the differences disappeared. Functional teat number of the AA. AB and BB gilts was 15.35 +/- 0.22, 15.53 +/- 0.18, and 15.60 +/- 0.29, respectively, and was not affected by PRLR genotype (P = 0.7). Functional teat number of piglets from AA, AB and BB mothers was 14.20 +/- 0.10, 14.37 +/- 0.08, and 14.63 +/- 0.13, respectively. Piglets from BB mothers had on average larger numbers of functional teats compared to piglets from AA mothers (P = 0.028). In conclusion, PRLR gene is a major gene or marker for age at first estrus, litter size, and litter average of number of functional teats in the Large White x Meishan F2 crossbred gilts studied. The favorable allele for litter size (A allele) is the unfavorable allele for age at first estrus and for litter mean of functional teat number.

Piglet and placental traits at term in relation to the estrogen receptor genotype in gilts.

Liveborn piglets from gilts with estrogen receptor (ESR) genotype AA (95 AA-AA and 91 AA-AB piglets), AB (88 AB-AA, 118 AB-AB, and 37 AB-BB piglets), and BB (97 BB-AB and 89 BB-BB piglets) were compared after farrowing, to examine whether piglet ESR genotype (ESRp) nested within maternal ESR genotype (ESRm) affected placental traits at term, piglet birth weight, and growth until weaning. Furthermore, the relation of birth weight to various placental traits and the relations between placental traits were evaluated relative to ESR genotype. For this study, 62 Large White x Meishan F2 crossbred gilts (18 AA, 24 AB, and 20 BB) were used. The gilts belonged to a population in which the A allele is favorable for litter size. ESRp nested within ESRm did not affect placental length, weight, surface area and number of areolae. ESRp nested within ESRm affected amnion weight (AA-AA amnions were heavier than AA-AB, AB-AA and BB-AB amnions), placental weight after including placental surface area in the model (AA-AB placentae were lighter than AA-AA, AB-BB and BB-AB placentae), placental efficiency calculated as birth weight divided by placental weight (AB-AA placentae were less efficient than AA-AB placentae), and the relations of birth weight to placental weight and birth weight to number of areolae. The found differences imply an interaction of maternal and fetal ESR genotype on placental traits (especially weight and number of areolae) during fetal development. Furthermore, the found effects on placental and amnion weight might be the result of a difference in thickness or vascularization or both. The favorable ESR allele for litter size, i.e. the A allele, appears to be the unfavorable allele for pre-weaning piglet growth. Therefore, further research on ESR in relation to vascularization, weight and thickness of placentae. uterine size, endometrial gland development, and piglet growth is recommended.

Parturition in gilts: duration of farrowing, birth intervals and placenta expulsion in relation to maternal, piglet and placental traits.

Large White x Meishan F2 crossbred gilts (n = 57) were observed continuously during farrowing while the placentae of their offspring were labeled in order to examine the duration of farrowing and placenta expulsion in relation to maternal-, piglet- and placental traits and the duration of birth interval in relation to birth weight, birth order and placental traits. Independently from each other, litter size, gestation length and offspring directed aggression significantly (P 0.05) affected duration of farrowing. An increase in litter size was associated with an increase of duration of farrowing and an increase in gestation length was associated with a decrease of duration of farrowing. Aggressive gilts took longer to farrow, compared to non-aggressive ones. After taking into account litter size, gestation length and offspring directed aggression, placental thickness (i.e., placental weight corrected for placental surface area) was significantly (P < 0.05) related to duration of farrowing, i.e., litters with on average thicker placentae took longer to farrow. The latter effect is the result of the fact that individual placental thickness significantly (P < 0.01) affected individual birth interval, independent of birth weight. The piglet has to break its own membranes to be able to start its journey through the uterus towards the birth channel. Apparently, a thicker placenta offers more resistance and thus prolongs the process of birth. Independent of placental thickness, birth interval significantly (P < 0.01) decreased with an increase in birth order (first born to last born). The high variation of birth intervals for the last born piglets, caused a slight increase in average birth interval for the latter piglets. Litters with on average more areolae per placenta took significantly (P < 0.001) less time to be born than litters with on average less areolae per placenta (independent of total number of piglets born and other placental traits), while birth intervals within litters were not affected by this trait. Thus, these results are probably due to a gilt trait rather than a piglet trait. Since the number of areolae represent the number of uterine glands present, the gilt trait might be uterine development. Duration of placenta expulsion significantly (P < 0.01) increased with an increase of duration of farrowing. Furthermore, the first placenta was expelled significantly (P < 0.01) earlier relative to last piglet when duration of farrowing was protracted, while there was no relation of the time interval between first placenta and last piglet and the duration of placenta expulsion. In conclusion, the most important finding of this study is that placental thickness rather than birth weight appears to play an important role in the duration of birth intervals and as a result, of duration of parturition in gilts.

The effect of estrogen receptor genotype on litter size and placental traits at term in F2 crossbred gilts.

The effect of estrogen receptor (ESR) genotype (two alleles, A and B) on litter size of 275 Large White x Meishan F2 crossbred gilts (73 AA, 126 AB and 76 BB gilts) was tested. In addition, for 63 of these gilts (18 AA, 24 AB, and 21 BB) the effect of ESR genotype on average placental traits at term was tested, since individual placental information was available for 88% of the 628 liveborn piglets. Without affecting average birth weight of the piglets, ESR genotype significantly affected litter size, i.e. AB gilts had larger litters than BB gilts (P < 0.05). Total number born was 11.38+/-0.38, 11.88+/-0.28, and 10.68+/-0.35, while number born alive was 10.45+/-0.39, 11.07+/-0.29, and 9.85+/-0.36 for AA, AB and BB gilts, respectively. Since the B allele in previous research was associated with largest litters, the hypothesis that ESR is a marker rather than the major gene itself is discussed. Average placental length, surface area, and weight including and excluding amnion were not affected by ESR genotype. However, placentae of AB gilts had a significantly lower number of areolae per placenta than BB gilts and had a lower number of areolae/cm2 placenta than AA and BB gilts. Number of areolae was 8945+/-663, 7240+/-619, and 9694+/-633, for AA, AB and BB gilts, respectively. Although the reason for the low number of areolae on placentae in AB gilts is not yet known, the results suggest that the ESR linked major gene for litter size might be involved in the development and activity of endometrial glands.

Components of litter size in gilts with different prolactin receptor genotypes.

Behavioral estrus and components of litter size at Day 35/36 of pregnancy were studied in gilts with prolactin receptor (PRLR) genotype AA (n=9), AB (n=25), and BB (n=22). This PRLR polymorphism (two alleles, A and B) has been associated with litter size, although it is not known whether the polymorphism itself causes differences in litter size or whether it is a marker for a closely linked causative gene. Estrus length in three successive estrous cycles was not affected by genotype, but estrous cycle length tended (P<0.1) to be longer for AA gilts compared to AB and BB gilts. AA gilts had a significantly (P<0.05) higher ovulation rate (21.5+/-0.9) than BB gilts (18.7+/-0.6), resulting in a numerically higher number of embryos at Day 35/36 (17.0+/-1.3, 15.6+/-0.8, and 13.7+/-0.9 for AA, AB, and BB gilts, respectively) which may lead to a subsequent difference in litter size. Ovulation rate of AB gilts (20.0+/-0.5) was intermediate. Genotype affected the total weight of the ovaries (P<0.05). Even after subtraction of the total weight of corpora lutea, ovarian weight in AA gilts was highest (16.6+/-1.0 g), in BB lowest (13.4+/-0.6g), and in AB gilts intermediate (15.0+/-0.6g; P<0.05). Unlike AB gilts, in AA and BB gilts uterine length was adapted to litter size, which led to longer (P<0.05) uteri for AA gilts (669+/-28 cm) compared to BB gilts (566+/-18 cm). Furthermore, embryos of AA gilts had heavier placentae (52.5+/-3.4 g) and larger implantation surface areas (309+/-19 cm(2)) than embryos of BB (42.0+/-2.3g, P<0.05; 256+/-12 cm(2), P<0.1) or AB (43.2+/-2.0 g, P<0.1; 257+/-11 cm(2), P<0.05) gilts. Results of this experiment show that the PRLR gene or a very closely linked gene affects porcine ovaries, uterus, and placenta in a way that might lead to differences in litter size. Since other genes and also environmental factors, however, might change the effect within the 112 days to parturition, it is preferable to state that the PRLR gene is a candidate gene for ovulation rate rather than for litter size.

Association of leptin gene polymorphisms with serum leptin concentration in dairy cows.

Leptin is a hormone produced by adipocytes, and its expression is regulated by body fatness and energy balance. This study describes the association of four leptin gene polymorphisms in dairy cows (R4C, A59V, RFLP1, and BM1500) with circulating leptin concentrations during the periparturient period. A59V is located at a between-species conserved region of leptin, and R4C might have effect on the tertiary structure of the leptin protein because of the presence of an extra cystein. RFLP1 is an intronic SNP and BM1500 is a microsatellite located 3.6 kb downstream of the leptin locus. The four polymorphisms were genotyped in 323 HF heifers with known pedigree. Leptin concentrations were determined biweekly from 30 days before until 80 days after parturition. The effect of genotype on leptin concentrations was modeled by fitting a spline in ASREML describing leptin concentrations as a function of days relative to parturition for each genotype/allele. Surprisingly, associations were found during pregnancy, but not during lactation. This indicates that the polymorphism could be more effective during pregnancy. If further studies demonstrate that more leptin-binding protein (Ob-Re) is present in this stage, it is hypothesized that a structural difference in the leptin protein could cause a sub-optimal binding stringency to Ob-Re. Free leptin could be cleared faster than bound leptin, and this could result in lower leptin concentrations during pregnancy for the polymorphism. The effects found might be ascribed to R4C. However, more study on the Ob-Re receptor, like binding stringencies between R4C and wild-type leptin and glycosylation during pregnancy, would provide more insight in the results found.