2006 Abstracts - American Society of Animal Science

7.83 BA. At Generation 16, responses in Line IOL relative to Line C2were 2.08 OR, 2.64 FF, and 1.68 BA; responses in Line COL were 2.32OR, 2.16 FF, and 1.92 BA. Line means at Generation 23 were: L45 =13.2 FF and 11.4 BA, Line C2 = 8.63 FF and 7.91 BA. With the OR/UCmodel, predicted UC in Lines IOL, COL, and C2 at Generation 16 were16.3, 15.6, and 10.5 fetuses, respectively. Responses in UC in latergenerations cannot be predicted because OR was not recorded. Balancingselection for OR and UC to increase LS based on the OR/UC modelappears to be more effective than index selection for OR and ES or directselection for LS. Direct LS selection is expected to be most effective inpopulations with high mean OR but average LS. QTL scans in theselines have identified one chromosomal position affecting OR and 14others affecting FF, BA, or numbers of mummified and stillborn piglets.Key Words: Pigs, Selection, Litter size95 What we have learned about prenatal physiology in the pigfrom uterine crowding experiments. J. Vallet*, B. Freking, J. P.Kayser, R. Christenson, and K. Leymaster, USDA, ARS, Roman L.Hruska U.S. Meat Animal Research Center, Clay Center, NE.The factor most limiting to litter size is becoming uterine capacity, thenumber of fetuses that the uterus can maintain until farrowing. Intrauterinecrowding does not appreciably limit litter size until after day 30of gestation, with most fetal loss occurring between day 30 and 40 ofgestation, although further losses occur in later gestation. We have usedunilateral hysterectomy-ovariectomy (UHO) to study the effects ofintrauterine crowding on the uterus, fetus and placenta. Studies indicatedfew effects on uterine function, measured as endometrial proteinsecretion. In UHO gilts, fetal hematocrits decreased with fetal weight,suggesting that small fetuses were anemic. This observation led to thediscovery of a polymorphism in the porcine erythropoietin receptorgene that is associated with litter size. Fetal brain growth is relativelyresistant to intrauterine crowding, particularly during late gestation. Incontrast, growth of the fetal heart is more resistant to crowding duringearly pregnancy. Further work on the mechanisms that shunt nutrientsto various organs could provide improvements in litter size. Finally,several previous studies indicate that placental efficiency (fetalweight:placental weight ratio) increased due to intrauterine crowding.Other studies suggest that placental folding may influence the efficiencyof the placenta. The depth of placental folding increased in placentasassociated with the smallest fetus in a litter. This occurred at the expenseof the fetal stroma layer surrounding the placental interface. Duringlate gestation in some small fetuses, the placenta may have no furtherroom to increase folding, potentially resulting in death. This couldexplain fetal losses due to intrauterine crowding that occur during lategestation. In summary, although the full effects of intrauterine crowdingare still unclear, clues are beginning to unfold that could result in improvementsin litter size in swine.Key Words: Uterus, Placenta, Fetus96 Fetal programming: what do we know and what are theimplications for the swine industry? R. Anthony* 1,2 , 1 ColoradoState University, Fort Collins, 2 University of Colorado Health SciencesCenter, Aurora.The concept of “fetal programming” or the “fetal origins of adult disease”hypothesis originated with extensive epidemiological studies ofvarious human populations. It is now well documented that growthrestrictedinfants, or infants of normal birth weights that experience analtered growth trajectory sometime during gestation, have a greater predispositionfor coronary heart disease, hypertension, obesity, and type2 diabetes as adults. These disease states are inter-related, and collectivelythey have been designated as the Metabolic Syndrome. Fetalgrowth restriction can result from a variety of causes, the majority ofwhich cause functional placental insufficiency and a failure to provideadequate nutrition to the developing fetus. Consequently, growth-restrictedfetuses are often hypoglycemic, hypoinsulinemic and hypoxic,and in more severe cases the fetus is also hypertensive and acidemic.Impaired organ growth and development, particularly with the abdominalorgans, occurs in these individuals, altering postnatal growth ratesand metabolic regulation as these offspring age. While these adult diseasestates are not often a concern in livestock production, altered metabolichomeostasis as a result of impaired fetal growth may well impactlivestock production efficiency. A number of animal models, primarilyin rodents and sheep, have been developed and used to investigate fetalgrowth restriction and the postnatal consequences, providing considerableinsight into the fetal and postnatal manifestation of fetal growthrestriction and the development of the metabolic syndrome. While pigshave not been used as extensively as sheep and rodents, recent studiescomparing low-birthweight (1.5 kg) pigsprovide evidence for “fetal programming” and its impact on adult metabolism.Low-birthweight pigs exhibit altered juvenile cardiovascularfunction, impaired glucose tolerance and insulin resistance as adults, aswell as increased adult fat depth. These results suggest impaired fetalgrowth may well have a significant impact on growth and compositionof swine, thereby impacting the efficiency of swine production.Key Words: Swine, Fetal growth restriction, Metabolic syndromeDairy Extension Symposium - Starch Utilization by Ruminants97 Laboratory methods of analysis for feedstuff starch contentand availability. M. B. Hall*, U. S. Dairy Forage Research Center,USDA-ARS, Madison, WI.The relationships that starch has with profitable production or withhealth disorders in cattle advise closer accounting of its quantity andquality in diets. Native starch is an Α-(1-4)-linked-glucan with Α-(1-6)linked branch points found in crystalline granules in plants. In feedstuffs,it can be analyzed by enzymatic hydrolysis, or by polarimetry, thoughboth suffer from interferences. Analysis by enzymatic hydrolysis requiresgelatinization, hydrolysis with enzymes specific for starch anddetection of glucose. Gelatinization breaks hydrogen bonds and the32