Prenatal programming of postnatal productivity and health of livestock: a brief review

2006 ◽  
Vol 46 (7) ◽  
pp. 725 ◽  
Author(s):  
A. W. Bell
Keyword(s):  
Large Body ◽  
Late Pregnancy ◽  
Later Life ◽  
High Energy ◽  
Meat Production ◽  
Postnatal Life ◽  
Large Animal ◽  
Fetal Life ◽  
Fetal Origins ◽  
Maternal Undernutrition

Human epidemiological evidence has suggested that metabolic perturbations during fetal life may increase predisposition to cardiovascular disease, type 2 diabetes and obesity in later life. A growing number of controlled experiments on sheep and other large animal species are adding to the already large body of experimental evidence from rat studies in supporting the ‘fetal origins’ hypothesis. Of particular practical relevance are findings that maternal undernutrition in late pregnancy can predispose lambs to glucose intolerance and increased adiposity in early adulthood. This effect may be exacerbated by high energy intakes and limited capacity for muscle growth in undernourished or growth-retarded lambs during early postnatal life. Recent Australian studies have demonstrated the effects of prenatal nutrition on postnatal growth and meat production in beef cattle, and on quantity and quality of wool production in sheep.

scholarly journals Impact of maternal undernutrition and fetal number on glucocorticoid, growth hormone and insulin-like growth factor receptor mRNA abundance in the ovine fetal kidney

Reproduction ◽  
2005 ◽  
Vol 129 (2) ◽  
pp. 151-159 ◽  
Author(s):  
K A Brennan ◽  
G S Gopalakrishnan ◽  
L Kurlak ◽  
S M Rhind ◽  
C E Kyle ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Kidney Development ◽  
Nutrient Deficiency ◽  
Growth Factor Receptor ◽  
Later Life ◽  
Mrna Abundance ◽  
Control Group ◽  
Fetal Life ◽  
Fetal Kidney ◽  
Maternal Undernutrition

Epidemiological and animal studies strongly indicate that the environment experienced in utero determines, in part, an individual’s likelihood of developing cardiovascular disease in later life. This risk has been further linked to impaired kidney function, as a result of compromised development during fetal life. The present study therefore examined the influence of maternal nutrient restriction (NR), targeted at specific periods of kidney development during early to mid gestation, on the mRNA abundance of receptors for glucocorticoid (GCR), growth hormone (GHR) and insulin-like growth factors-I (IGF-IR) and -II (IGF-IIR), and the IGF-I and -II ligands. This was undertaken in both singleton and twin fetuses. At conception ewes were randomly allocated to either an adequately fed control group or one of four nutrient-restricted groups that were fed half the control amount from 0 to 30, 31 to 65, 66 to110 or 0 to110 days gestation. At 110 days gestation all ewes were humanely euthanased and fetal kidneys and surrounding adipose tissue sampled. There was no effect of NR or fetal number on kidney weight, shape or nephron number, but the surrounding fat mass was increased in singleton fetuses exposed to NR for 110 days. An increase in kidney mRNA abundance with NR only occurred in singleton fetuses where IGF-IR mRNA was enhanced with NR from 66–110 days gestation. In twin fetuses, NR had no effect on mRNA abundance. However, for all genes examined mRNA expression was lower in the kidneys of twin compared with singleton fetuses following NR, and the magnitude of the effect was dependent on the timing of NR. In conclusion, the abundance of mRNA for receptors which regulate fetal kidney development are lower in twin animals compared with singletons following periods of nutrient deficiency. This may impact on later kidney development and function.

scholarly journals Maternal nutrient restriction in late pregnancy programs postnatal metabolism and pituitary development in beef heifers

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0249924
Author(s):  
John M. Long ◽  
Levi A. Trubenbach ◽  
Kenneth C. Hobbs ◽  
Andrew E. Poletti ◽  
Chelsie B. Steinhauser ◽  
...  
Keyword(s):  
Area Under The Curve ◽  
Late Pregnancy ◽  
Postnatal Growth ◽  
Late Gestation ◽  
Nutrient Restriction ◽  
Postnatal Life ◽  
Beef Heifers ◽  
Maternal Undernutrition ◽  
Ad Libitum

Maternal undernutrition during pregnancy followed by ad libitum access to nutrients during postnatal life induces postnatal metabolic disruptions in multiple species. Therefore, an experiment was conducted to evaluate postnatal growth, metabolism, and development of beef heifers exposed to late gestation maternal nutrient restriction. Pregnancies were generated via transfer of in vitro embryos produced using X-bearing sperm from a single Angus sire. Pregnant dams were randomly assigned to receive either 100% (control; n = 9) or 70% (restricted; n = 9) of their total energy requirements from gestational day 158 to parturition. From post-natal day (PND) 301 until slaughter (PND485), heifers were individually fed ad libitum in a Calan gate facility. Calves from restricted dams were lighter than controls at birth (P<0.05) through PND70 (P<0.05) with no difference in body weight from PND105 through PND485 (P>0.10). To assess pancreatic function, glucose tolerance tests were performed on PND315 and PND482 and a diet effect was seen with glucose area under the curve being greater (P<0.05) in calves born to restricted dams compared to controls. At slaughter, total internal fat was greater (P<0.05) in heifers born to restricted dams, while whole pituitary weight was lighter (P<0.05). Heifers from restricted dams had fewer growth hormone-positive cells (somatotrophs) compared to controls (P<0.05). Results demonstrate an impaired ability to clear peripheral glucose in heifers born to restricted dams leading to increased deposition of internal fat. A reduction in the number of somatotrophs may contribute to the adipogenic phenotype of heifers born to restricted dams due to growth hormone’s known anabolic roles in growth, lipolysis, and pancreatic islet function.

Effects of maternal undernutrition during late gestation and/or lactation on colostrum synthesis and immunological parameters in the offspring

2016 ◽  
Vol 28 (3) ◽  
pp. 384 ◽  
Author(s):  
S. Chadio ◽  
A. Katsafadou ◽  
B. Kotsampasi ◽  
G. Michailidis ◽  
K. C. Mountzouris ◽  
...  
Keyword(s):  
Immune System ◽  
Quantitative Polymerase Chain Reaction ◽  
Later Life ◽  
Polymerase Chain Reaction Analysis ◽  
Late Gestation ◽  
Fetal Life ◽  
Immunological Parameters ◽  
Maternal Undernutrition ◽  
Pregnancy And Lactation ◽  
Polymerase Chain

The emerging immune system is vulnerable to insult not only during fetal life, but also through colostrum transfer of maternal factors with immunomodulatory functions. The aim of the present study was to examine the effects of maternal undernutrition during late gestation and/or lactation on colostrum and milk synthesis, as well as on immunological parameters in offspring. Pregnant ewes were fed to 100% of nutrient requirements throughout pregnancy and lactation (Control) or to 50% during lactation (R1) or during the last 20 days of pregnancy and lactation (R2). Colostrum samples were collected 3 and 18 h after parturition and thymus glands were obtained from 5-month-old offspring. Lamb birthweight did not differ between groups, whereas growth rate was significantly lower in males in the R1 group and in females in both undernourished groups. There was a significant reduction in lactose percentage in the 18-h colostrum of the R2 group. The IgG concentration, as a percentage of protein, was significantly increased in 3-h colostrum samples of the R2 group. Quantitative polymerase chain reaction analysis revealed a significant increase in the expression of Toll-like receptor (TLR) 2, TLR4 and TLR9 in the thymus gland of female lambs in both undernourished groups. In conclusion, early life nutritional imbalances may impact on immune system function in later life due to programming effects.

Cardiovascular and hypothalamic-pituitary-adrenal axis development in late gestation fetal sheep and young lambs following modest maternal nutrient restriction in early gestation

2000 ◽  
Vol 12 (8) ◽  
pp. 443 ◽  
Author(s):  
P. Hawkins ◽  
C. Steyn ◽  
H. H. G. McGarrigle ◽  
N. A. Calder ◽  
T. Saito ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Hpa Axis ◽  
Femoral Artery ◽  
Cardiovascular Response ◽  
Late Gestation ◽  
Postnatal Life ◽  
Fetal Life ◽  
Fetal Sheep ◽  
Hypothalamic Pituitary Adrenal ◽  
Maternal Undernutrition

The effect of a 15% reduction in maternal nutrition for the first 70 days of gestation on cardiovascular and hypothalamic–pituitary–adrenal (HPA) axis responses to administration of corticotropin releasing hormone (CRH) + arginine vasopressin (AVP) was studied at 128 0.7 days gestation in fetal sheep and postnatally, at 85 4.5 days in young lambs. The effect on the fetal cardiovascular response to acute hypoxaemia was also examined. Under basal conditions, fetal heart rate (FHR) was reduced (P<0.05) and basal femoral artery vascular resistance (FVR) was increased (P<0.05) in fetuses of dietary-restricted (R) ewes compared with controls (C). Fetal mean arterial pressure (MAP) was similar in both groups. Femoral artery vascular resistance was also greater during hypoxaemia in R fetuses compared with C fetuses (P<0.05), suggesting that chemoreflex mechanisms were augmented in the R group. The fetal ACTH response to CRH + AVP was similar in both groups. However, cortisol responses to CRH + AVP were smaller in R fetuses compared with C fetuses (P<0.05). Postnatally, basal MAP (P<0.05), and ACTH (P<0.01) and cortisol (P<0.001) responses were greater in R lambs compared with C lambs. It was concluded that modest maternal undernutrition during pregnancy alters development of the cardiovascular system, producing elevated blood pressure in postnatal life. Development of the HPA axis is also altered, with reduced activity during fetal life, but increased activity postnatally. The data suggest that the HPA axis may play a role in mediating the elevation of MAP in R lambs.

scholarly journals Effects of Prenatal Exposure to the Dutch Famine on Adult Disease in Later Life: An Overview

Twin Research ◽  
2001 ◽  
Vol 4 (5) ◽  
pp. 293-298 ◽  
Author(s):  
Tessa J. Roseboom ◽  
Jan H.P. van der Meulen ◽  
Anita C.J. Ravelli ◽  
Clive Osmond ◽  
David J.P. Barker ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Plasma Concentrations ◽  
Later Life ◽  
Factor Vii ◽  
Long Term Effects ◽  
Fetal Origins ◽  
Maternal Undernutrition ◽  
Fetal Origins Hypothesis ◽  
Increased Risk

AbstractPeople who were small at birth have been shown to have an increased risk of CHD and chronic bronchitis in later life. These findings have led to the fetal origins hypothesis that proposes that the fetus adapts to a limited supply of nutrients, and in doing so it permanently alters its physiology and metabolism, which could increase its risk of disease in later life. The Dutch famine — though a historical disaster — provides a unique opportunity to study effects of undernutrition during gestation in humans. People who had been exposed to famine in late or mid gestation had reduced glucose tolerance. Whereas people exposed to famine in early gestation had a more atherogenic lipid profile, somewhat higher fibrinogen concentrations and reduced plasma concentrations of factor VII, a higher BMI and they appeared to have a higher risk of CHD. Though the latter was based on small numbers, as could be expected from the relatively young age of the cohort. Nevertheless, this is the first evidence in humans that maternal undernutrition during gestation is linked with the risk of CHD in later life. Our findings broadly support the hypothesis that chronic diseases originate through adaptations made by the fetus in response to undernutrition. The long-term effects of intrauterine undernutrition, however, depend upon its timing during gestation and on the tissues and systems undergoing critical periods of development at that time. Furthermore, our findings suggest that maternal malnutrition during gestation may permanently affect adult health without affecting the size of the baby at birth. This gives the fetal origins hypothesis a new dimension. It may imply that adaptations that enable the fetus to continue to grow may nevertheless have adverse consequences for health in later life. CHD may be viewed as the price paid for successful adaptations to an adverse intra-uterine environment. It also implies that the long-term consequences of improved nutrition of pregnant women will be underestimated if these are solely based on the size of the baby at birth. We need to know more about what an adequate diet for pregnant women might be. In general, women are especially receptive to advice about diet and lifestyle before and during a pregnancy. This should be exploited to improve the health of future generations.

Early metabolic alterations in edematous perihematomal brain regions following experimental intracerebral hemorrhage

1998 ◽  
Vol 88 (6) ◽  
pp. 1058-1065 ◽  
Author(s):  
Kenneth R. Wagner ◽  
Guohua Xi ◽  
Ya Hua ◽  
Marla Kleinholz ◽  
Gabrielle M. de Courten-Myers ◽  
...  
Keyword(s):  
White Matter ◽  
Intracerebral Hemorrhage ◽  
Gray Matter ◽  
High Energy ◽  
Brain Regions ◽  
Large Animal ◽  
High Energy Phosphate ◽  
Content Type ◽  
Water Contents ◽  
Fine Print

Object. The authors previously demonstrated, in a large-animal intracerebral hemorrhage (ICH) model, that markedly edematous (“translucent”) white matter regions (> 10% increases in water contents) containing high levels of clotderived plasma proteins rapidly develop adjacent to hematomas. The goal of the present study was to determine the concentrations of high-energy phosphate, carbohydrate substrate, and lactate in these and other perihematomal white and gray matter regions during the early hours following experimental ICH. Methods. The authors infused autologous blood (1.7 ml) into frontal lobe white matter in a physiologically controlled model in pigs (weighing approximately 7 kg each) and froze their brains in situ at 1, 3, 5, or 8 hours postinfusion. Adenosine triphosphate (ATP), phosphocreatine (PCr), glycogen, glucose, lactate, and water contents were then measured in white and gray matter located ipsi- and contralateral to the hematomas, and metabolite concentrations in edematous brain regions were corrected for dilution. In markedly edematous white matter, glycogen and glucose concentrations increased two- to fivefold compared with control during 8 hours postinfusion. Similarly, PCr levels increased several-fold by 5 hours, whereas, except for a moderate decrease at 1 hour, ATP remained unchanged. Lactate was markedly increased (approximately 20 µmol/g) at all times. In gyral gray matter overlying the hematoma, water contents and glycogen levels were significantly increased at 5 and 8 hours, whereas lactate levels were increased two- to fourfold at all times. Conclusions. These results, which demonstrate normal to increased high-energy phosphate and carbohydrate substrate concentrations in edematous perihematomal regions during the early hours following ICH, are qualitatively similar to findings in other brain injury models in which a reduction in metabolic rate develops. Because an energy deficit is not present, lactate accumulation in edematous white matter is not caused by stimulated anaerobic glycolysis. Instead, because glutamate concentrations in the blood entering the brain's extracellular space during ICH are several-fold higher than normal levels, the authors speculate, on the basis of work reported by Pellerin and Magistretti, that glutamate uptake by astrocytes leads to enhanced aerobic glycolysis and lactate is generated at a rate that exceeds utilization.

The effect of level and pattern of energy intake during late pregnancy on the performance of housed Scottish Blackface ewes

1973 ◽  
Vol 16 (2) ◽  
pp. 165-171 ◽  
Author(s):  
T. H. McClelland ◽  
T. J. Forbes
Keyword(s):  
Body Weight ◽  
Energy Intake ◽  
Post Partum ◽  
Body Weight Loss ◽  
Late Pregnancy ◽  
High Energy ◽  
Metabolizable Energy ◽  
Feeding Period ◽  
Total Period ◽  
Constant Energy

SUMMARYSixty Scottish Blackface ewes were used in a 2 × 2 factorial experiment in which two levels of metabolizable energy (ME) were given during the final 6 weeks of pregnancy. In two treatments 1600 and 2000 kcal M E were given daily over the total period while in the remaining treatments daily ME intakes were 1200 and 1600 kcal ME during the first 3 weeks of the feeding period and 2000 and 2400 kcal ME during the last 3 weeks. Digestible crude protein (DCP) intakes were constant at approximately 30 g per head daily in the constant energy treatments and 15 and 45 g per head daily in the first and second periods respectively for the low-high energy treatments.Energy intake had no statistically significant effect on lamb birth weight nor on ewe net body-weight change (change from the start of the experimental feeding period to immediately post partum). Ewes on low-high energy intakes had a significantly lower net body-weight loss than did ewes on constant energy intakes. Pattern of feeding had no significant effect on lamb birth weights. Negative nitrogen balances were found during the first feeding period where the daily DCP intake was approximately 15 g per head.

Nutritional programming and the reproductive function of the offspring

2014 ◽  
Vol 54 (9) ◽  
pp. 1166 ◽  
Author(s):  
P. Chavatte-Palmer ◽  
C. Dupont ◽  
N. Debus ◽  
S. Camous
Keyword(s):  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Maternal Nutrition ◽  
Reproductive Function ◽  
Fetal Life ◽  
Ample Evidence ◽  
Primordial Follicles ◽  
Intrauterine Growth ◽  
Maternal Undernutrition ◽  
Males And Females

There is ample evidence on the importance of maternal nutrition during pregnancy on fetal and offspring development. In ruminant females, the pool of oocytes is complete and definitive before birth, based on the resting reserve of primordial follicles established during fetal life, which represent the lifespan supply for the female’s fertilisable oocytes, whereas in males, although the production of spermatozoa is a continuous process throughout post-pubertal life. Sertoli cells, which play a central role in the development of a functional testis, proliferate during pre- and post-natal life, coordinating testicular development. Both male and female fertility may, therefore, be affected by the maternal environment, but studies on the effects of developmental nutritional conditions on reproductive function and fertility, both in males and females, are relatively scarce. In humans, intrauterine growth retardation has been associated with abnormal ovarian development, characterised by a decreased volume of primordial follicles in the ovarian cortical tissue in girls, and a higher incidence of cryptorchidism in boys, with subsequent low sperm counts in adulthood. Age at puberty and gonadotropin and inhibin B plasma concentrations are also affected. Animal studies suggest both in males and females that maternal undernutrition during pregnancy may affect pituitary response to GnRH and gonadal development and function, depending on the timing and magnitude of the undernutrition. Excess nutrition, which is often associated with intrauterine growth retardation in domestic species, induces effects on the onset of puberty and both testicular and ovarian function, maybe through the observed reduction in fetal growth. This review addresses the influence of maternal nutrition on offspring reproductive function using examples in humans and animals, with particular focus on ruminants.

scholarly journals Detecting the Effects of Early-Life Exposures: Why Fecundity Matters

2019 ◽  
Author(s):  
Jenna Nobles ◽  
Amar Hamoudi
Keyword(s):  
Infant Health ◽  
Statistical Significance ◽  
Absolute Magnitude ◽  
Later Life ◽  
Contrast Effects ◽  
Fetal Origins ◽  
Health Trajectories ◽  
Maternal And Infant Health ◽  
Selective Survival ◽  
Early Life Exposures

Prenatal exposures have meaningful effects on health across the lifecourse. Innovations in causal inference have shed new light on these effects. Here, we motivate the importance of innovation in the characterization of fecundity, and prenatal selection in particular. We argue that such innovation is crucial for expanding knowledge of the fetal origins of later life health. Pregnancy loss is common, responsive to environmental factors, and closely related to maternal and fetal health outcomes. As a result, selection into live birth is driven by many of the same exposures that shape the health trajectories of survivors. Lifecourse effects that are inferred without accounting for these dynamics may be significantly distorted by survival bias. We use a set of Monte Carlo simulations with realistic parameters to examine the implications of prenatal survival bias. We find that even in conservatively specified scenarios, true fetal origin effects can be underestimated by 50% or more. In contrast, effects of exposures that reduce the probability of prenatal survival but improve the health of survivors will be overestimated. The absolute magnitude of survival bias can even exceed small effect sizes, resulting in inferences that beneficial exposures are harmful or vice-versa. We also find reason for concern that moderately sized true effects, underestimated due to failure to account for selective survival, are missing from scientific knowledge because they do not clear statistical significance filters. This bias has potential real-world costs; policy decisions about interventions to improve maternal and infant health will be affected by underestimated program impact.

scholarly journals Minireview: Epigenetic Programming of Diabetes and Obesity: Animal Models

Endocrinology ◽  
2012 ◽  
Vol 153 (3) ◽  
pp. 1031-1038 ◽  
Author(s):  
Yoshinori Seki ◽  
Lyda Williams ◽  
Patricia M. Vuguin ◽  
Maureen J. Charron
Keyword(s):  
Metabolic Disease ◽  
Animal Models ◽  
Posttranslational Modifications ◽  
Cytosine Methylation ◽  
Metabolic Diseases ◽  
Later Life ◽  
Epigenetic Modifications ◽  
Micro Rna ◽  
Fetal Origins ◽  
Diabetes And Obesity

A growing body of evidence suggests that the intrauterine (IU) environment has a significant and lasting effect on the long-term health of the growing fetus and the development of metabolic disease in later life as put forth in the fetal origins of disease hypothesis. Metabolic diseases have been associated with alterations in the epigenome that occur without changes in the DNA sequence, such as cytosine methylation of DNA, histone posttranslational modifications, and micro-RNA. Animal models of epigenetic modifications secondary to an altered IU milieu are an invaluable tool to study the mechanisms that determine the development of metabolic diseases, such as diabetes and obesity. Rodent and nonlitter bearing animals are good models for the study of disease, because they have similar embryology, anatomy, and physiology to humans. Thus, it is feasible to monitor and modify the IU environment of animal models in order to gain insight into the molecular basis of human metabolic disease pathogenesis. In this review, the database of PubMed was searched for articles published between 1999 and 2011. Key words included epigenetic modifications, IU growth retardation, small for gestational age, animal models, metabolic disease, and obesity. The inclusion criteria used to select studies included animal models of epigenetic modifications during fetal and neonatal development associated with adult metabolic syndrome. Experimental manipulations included: changes in the nutritional status of the pregnant female (calorie-restricted, high-fat, or low-protein diets during pregnancy), as well as the father; interference with placenta function, or uterine blood flow, environmental toxin exposure during pregnancy, as well as dietary modifications during the neonatal (lactation) as well as pubertal period. This review article is focused solely on studies in animal models that demonstrate epigenetic changes that are correlated with manifestation of metabolic disease, including diabetes and/or obesity.

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