Reproductive loss in high-producing dairy cattle: where will it end?

Conceptus energy and nitrogen de- mands in late pregnancy are mostly met by placental uptake of maternal glucose and amino acids. The resulting 30 to 50% increase in maternal requirements for these nutrients is met partly by increased volun- tary intake and partly by an array of maternal metabolic adaptations. The latter include increased hepatic gluconeogenesis from endogenous substrates, decreased peripheral tissue glucose utilization, in- creased fatty acid mobilization from adipose tissue, and, possibly, increased amino acid mobilization from muscle. Within 4 d of parturition, mammary demands for glucose, amino acids, and fatty acids are several- fold those of the pregnant uterus before term. Even unusual postparturient increases in voluntary intake cannot satisfy this increased nutrient demand. There- fore, rates of hepatic gluconeogenesis and adipose fat mobilization are greatly accelerated. Concomitant changes in amino acid metabolism include increased hepatic protein synthesis and, possibly, decreased amino acid catabolism, and increased peripheral mobilization of amino acids. Insulin resistance in adipose tissue and muscle, developed during late pregnancy, continues postpartum; adipose lipolytic responsiveness and sensitivity to adrenergic agents are increased postpartum beyond their levels during late pregnancy. Before parturition, these homeorhetic adjustments may be coordinated with lactogenesis by increased secretion of estradiol and prolactin. Their amplification and reinforcement at and soon after parturition may be regulated mostly by somatotropin.

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Regulation of organic nutrient metabolism during transition from late pregnancy to early lactation

Transforming growth factor beta 1 (TGF beta 1) is shown here to be required for yolk sac haematopoiesis and endothelial differentiation. Mice with a targeted mutation in the TGF beta 1 gene were examined to determine the cause of prenatal lethality, which occurs in 50% of homozygous TGF beta 1 null (TGF beta 1-/-) conceptions. 50% of TGF beta 1-/- and 25% of TGF beta 1-+-) conceptions. 50% of TGF beta 1-/- and 25% of TGF beta 1+/- conceptuses were found to die at around 10.5 dpc. The primary defects were restricted to extraembryonic tissues, namely the yolk sac vasculature and haematopoietic system. The embryos per se showed developmental retardation, oedema and necrosis, which were probably secondary to the extraembryonic lesions. The defect in vasculogenesis appeared to affect endothelial differentiation, rather than the initial appearance and outgrowth of endothelial cells. Initial differentiation of yolk sac mesoderm to endothelial cells occurred, but defective differentiation resulted in inadequate capillary tube formation, and weak vessels with reduced cellular adhesiveness. Defective haematopoiesis resulted in a reduced erythroid cell number within the yolk sac. Defective yolk sac vasculogenesis and haematopoiesis were present either together, or in isolation of each other. The phenotypes are consistent with the observation of abundant TGF beta 1 gene expression in both endothelial and haematopoietic precursors. The data indicate that the primary effect of loss of TGF beta 1 function in vivo is not increased haematopoietic or endothelial cell proliferation, which might have been expected by deletion of a negative growth regulator, but defective haematopoiesis and endothelial differentiation.

Defective haematopoiesis and vasculogenesis in transforming growth factor-beta 1 knock out mice

Intrauterine growth retardation (IUGR), defined as impaired growth and development of the mammalian embryo/fetus or its organs during pregnancy, is a major concern in domestic animal production. Fetal growth restriction reduces neonatal survival, has a permanent stunting effect on postnatal growth and the efficiency of feed/forage utilization in offspring, negatively affects whole body composition and meat quality, and impairs long-term health and athletic performance. Knowledge of the underlying mechanisms has important implications for the prevention of IUGR and is crucial for enhancing the efficiency of livestock production and animal health. Fetal growth within the uterus is a complex biological event influenced by genetic, epigenetic, and environmental factors, as well as maternal maturity. These factors impact on the size and functional capacity of the placenta, uteroplacental blood flows, transfer of nutrients and oxygen from mother to fetus, conceptus nutrient availability, the endocrine milieu, and metabolic pathways. Alterations in fetal nutrition and endocrine status may result in developmental adaptations that permanently change the structure, physiology, metabolism, and postnatal growth of the offspring. Impaired placental syntheses of nitric oxide (a major vasodilator and angiogenic factor) and polyamines (key regulators of DNA and protein synthesis) may provide a unified explanation for the etiology of IUGR in response to maternal undernutrition and overnutrition. There is growing evidence that maternal nutritional status can alter the epigenetic state (stable alterations of gene expression through DNA methylation and histone modifications) of the fetal genome. This may provide a molecular mechanism for the role of maternal nutrition on fetal programming and genomic imprinting. Innovative interdisciplinary research in the areas of nutrition, reproductive physiology, and vascular biology will play an important role in designing the next generation of nutrient-balanced gestation diets and developing new tools for livestock management that will enhance the efficiency of animal production and improve animal well being.

Board-invited review: intrauterine growth retardation: implications for the animal sciences.

https://hal.archives-ouvertes.fr/hal-01173575/document

Invited review: Body condition score and its association with dairy cow productivity, health, and welfare

Partitioning of Nutrients During Pregnancy and Lactation: A Review of Mechanisms Involving Homeostasis and Homeorhesis

http://www.adisseo.biz/EM/documents/SmartMail/2000_JDairySci_Larson.pdf

Reduced fertility associated with low progesterone postbreeding and increased milk urea nitrogen in lactating cows.

Pregnant ewes were chronically exposed to thermoneutral (TN; 20 degrees C, 30% relative humidity) or hot (H; 40 degrees C 9 h/d, 30 degrees C 15 h/d, 40% relative humidity) environments between d 64 and 136 to 141 of pregnancy. They were sampled for blood at 14-d intervals during this period for measurement of plasma metabolites and hormones, then slaughtered and dissected to measure conceptus weights, dimensions and fetal organ weights. Rectal temperatures of H ewes were elevated .3 to 1.0 C degrees above those of TN ewes throughout the experiment. Voluntary feed intakes were not altered by heat exposure except after 120 d of pregnancy, when feed intake was about 25% lower (P less than .10) by H than by TN ewes. Blood 3-hydroxybutyrate concentrations were not affected by heat, but plasma glucose concentrations were greater in H than in TN animals after 120 d (P less than .05). Placental weight, reduced by 54% (P less than .001) by heat exposure of ewes, was correlated positively with fetal weight and correlated negatively with fetal/placental weight ratio, fetal brain/liver weight ratio and fetal relative heart weight. Late in pregnancy, plasma concentrations of progesterone, cortisol and placental lactogen were reduced (P less than .01) in H ewes, whereas triiodothyronine levels were markedly lower (P less than .03) at all stages of pregnancy. Plasma concentrations of prolactin were elevated dramatically (P less than .01) and a modest increase (P less than .03) in somatotropin levels was recorded in H ewes. These results are consistent with our hypothesis that heat-induced fetal growth retardation is secondary to a primary reduction in placental growth; this could be mediated partly by reduced peripheral activity of thyroid hormones. Heat-induced reductions in secretion of progesterone and ovine placental lactogen more likely were a consequence than a cause of placental stunting.

Chronic Heat Stress and Prenatal Development in Sheep: I. Conceptus Growth and Maternal Plasma Hormones and Metabolites

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Control of Parturition in Domestic Animals

Maturation-promoting factor (MPF) is known to be a key regulator of both mitotic and meiotic cell cycles MPF is a complex of a B cyclin and the cyclin-dependent kinase cdkl (p34cdc2) Oocyte maturation and its arrest at metaphase of meiosis II (MII) are regulated by changes in MPF activity In this study, experiments were conducted to examine the dynamics of MPF activity and its constituent proteins during in vitro maturation of bovine oocytes Bovine oocytes displayed relatively low levels of MPF (histone H1 kinase) activity at the germinal vesicle stage during the first 8 h of maturation MPF activity increased gradually thereafter, and its first peak of activity occurred at 12-14 h of maturation (presumptive metaphase I), which was followed by an abrupt reduction in activity at 16-18 h, during presumptive anaphase and telophase MPF activity then increased, reaching a plateau at 20-24 h of maturation (MII stage) This high level of MPF activity was maintained for several hours but decreased gradually after 30 h of maturation and became barely detectable by 48 h of in vitro maturation (IVM) culture At each time point, there was a significant variation among individual oocytes in histone H1 kinase activity, which was probably due to asynchronous maturation Abundance of cdk1 increased gradually during the first 8 h and then remained relatively constant except for an apparent reduction at 18-22 h of IVM The level of cyclin B2 increased quickly during the initial 2 h of culture, and this high level was maintained until 16 h, after which a significant reduction was observed between 18 and 22 h of IVM The de novo synthesis of cyclin B2, however, exhibited a biphasic oscillation during maturation, with peaks before the onset of MI and of MII These results have defined the profiles of MPF activity and its individual components during bovine oocyte maturation in vitro We conclude that active MPF regulates bovine oocyte maturation and that de novo synthesis of cyclin B2 occurs during the process of maturation

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W. B. Currie

Papers

Partitioning of Nutrients During Pregnancy and Lactation: A Review of Mechanisms Involving Homeostasis and Homeorhesis

Reduced fertility associated with low progesterone postbreeding and increased milk urea nitrogen in lactating cows.

Chronic Heat Stress and Prenatal Development in Sheep: I. Conceptus Growth and Maternal Plasma Hormones and Metabolites

Control of Parturition in Domestic Animals

Dynamics of maturation-promoting factor and its constituent proteins during in vitro maturation of bovine oocytes.