The Greater Proportion of Born-Light Progeny from Sows Mated in Summer Contributes to Increased Carcass Fatness Observed in Spring.

The backfat of pig carcasses is greater in spring than summer in Australia. The unexplained seasonal variation in carcass backfat creates complications for pig producers in supplying consistent lean carcasses. As a novel explanation, we hypothesised that the increased carcass fatness in spring was due to a greater percentage of born-light progeny from sows that were mated in summer and experienced hot conditions during early gestation. The first part of our experiment compared the birth weight of piglets born to the sows mated in summer (February, the Southern Hemisphere) with those born to sows mated in autumn (May; the Southern Hemisphere), and the second part of the experiment compared the growth performance and carcass fatness of the progeny that were stratified as born-light (0.7-1.1 kg) and born-normal (1.3-1.7 kg) from the sows mated in these two seasons. The results showed that the sows mated in summer experienced hotter conditions during early gestation as evidenced by an increased respiration rate and rectal temperature, compared with those mated in autumn. The sows mated in summer had a greater proportion of piglets that were born ≤1.1 kg (24.2% vs. 15.8%, p < 0.001), lower average piglet birth weight (1.39 kg vs. 1.52 kg, p < 0.001), lower total litter weights (18.9 kg vs. 19.5 kg, p = 0.044) and lower average placental weight (0.26 vs. 0.31 kg, p = 0.011) than those mated in autumn, although litter sizes were similar. Feed intake and growth rate of progeny from 14 weeks of age to slaughter (101 kg live weight) were greater for the born-normal than born-light pigs within the progeny from sows mated in autumn, but there was no difference between the born-light and normal progeny from sows mated in summer, as evidenced by the interaction between piglet birth weight and sow mating season (Both p < 0.05). Only the born-light piglets from the sows mated in summer had a greater backfat thickness and loin fat% than the progeny from the sows mated in autumn, as evidenced by a trend of interaction between piglet birth weight and sow mating season (Both p < 0.10). In conclusion, the increased proportion of born-light piglets (0.7-1.1 kg range) from the sows mated in summer contributed to the increased carcass fatness observed in spring.

Feeding Conjugated Linoleic Acid without a Combination of Medium-Chain Fatty Acids during Late Gestation and Lactation Improves Pre-Weaning Survival Rates of Gilt and Sow Progeny.

Feeding conjugated linoleic acid (CLA) or medium-chain fatty acids (MCFA) to dams has been shown to improve progeny growth and survival, and hence may be particularly advantageous to gilt progeny. Primiparous (n = 129) and multiparous sows (n = 123; parities 3 and 4) were fed one of four diets from day 107 of gestation (107.3 ± 0.1 days) until weaning (day 27.2 ± 0.1 of lactation): (i) control diet; (ii) 0.5% CLA diet; (iii) 0.1% MCFA diet; and (iv) equal parts of (ii) and (iii). Progeny performance data were collected and, from a subset of sows (n = 78) and their piglets (n = 144), a colostrum (day 0), milk (day 21), and piglet serum sample (day 3) were analyzed for immunoglobulin G and several selected metabolites. Liveborn pre-weaning mortality tended to be lowest (p = 0.051) in piglets from sows fed 0.5% CLA. However, sows fed the CLA diet had more (p = 0.005) stillbirths than those on the other diets. There were few effects of diet or the dam parity x diet interaction (p ≥ 0.05) on other parameters. Overall, feeding CLA or MCFA did not improve the performance of primiparous sows, multiparous sows, or their progeny.

Function of Wnt/ß-catenin in counteracting Tcf3 repression through the Tcf3-ß-catenin interaction.

The canonical Wnt/ß-catenin signaling pathway classically functions through the activation of target genes by Tcf/Lef-ß-catenin complexes. In contrast to ß-catenin-dependent functions described for Tcf1, Tcf4 and Lef1, the known embryonic functions for Tcf3 in mice, frogs and fish are consistent with ß-catenin-independent repressor activity. In this study, we genetically define Tcf3-ß-catenin functions in mice by generating a Tcf3ΔN knock-in mutation that specifically ablates Tcf3-ß-catenin. Mouse embryos homozygous for the knock-in mutation (Tcf3(ΔN/ΔN)) progress through gastrulation without apparent defects, thus genetically proving that Tcf3 function during gastrulation is independent of ß-catenin interaction. Tcf3(ΔN/ΔN) mice were not viable, and several post-gastrulation defects revealed the first in vivo functions of Tcf3-ß-catenin interaction affecting limb development, vascular integrity, neural tube closure and eyelid closure. Interestingly, the etiology of defects indicated an indirect role for Tcf3-ß-catenin in the activation of target genes. Tcf3 directly represses transcription of Lef1, which is stimulated by Wnt/ß-catenin activity. These genetic data indicate that Tcf3-ß-catenin is not necessary to activate target genes directly. Instead, our findings support the existence of a regulatory circuit whereby Wnt/ß-catenin counteracts Tcf3 repression of Lef1, which subsequently activates target gene expression via Lef1-ß-catenin complexes. We propose that the Tcf/Lef circuit model provides a mechanism downstream of ß-catenin stability for controlling the strength of Wnt signaling activity during embryonic development.