Effects of fetal genotype and sex on developmental response to maternal malnutrition

2017 ◽  
Vol 29 (6) ◽  
pp. 1155 ◽  
Author(s):  
Laura Cogollos ◽  
Consolacion Garcia-Contreras ◽  
Marta Vazquez-Gomez ◽  
Susana Astiz ◽  
Raul Sanchez-Sanchez ◽  
...  
Keyword(s):  
Adaptive Response ◽  
Essential Fatty Acids ◽  
Disease Status ◽  
Prenatal Development ◽  
Female Offspring ◽  
Large White ◽  
Maternal Malnutrition ◽  
Maternal Genotype ◽  
Show Evidence ◽  
Fetal Genotype

The present study aimed to determine whether developmental patterns, adiposity level and fatty-acid composition of fetuses exposed to maternal malnutrition are driven by their sex or their genotype, or both, as these may modulate the adaptive response to the intrauterine environment independently of the maternal genotype. We used a single maternal genotype (purebred Iberian (IB) sows), which was inseminated with heterospermic semen (obtained by mixing semen from Iberian and Large White (LW) boars), to obtain four different subsets of fetuses (male and female, purebred (IB × IB) and crossbred (IB × LW)) in Iberian purebred sows. Analysis of fetal phenotypes indicated a better adaptive response of the female offspring, which was modulated by their genotype. When faced with prenatal undernutrition, females prioritised the growth of vital organs (brain, liver, lungs, kidneys and intestine) at the expense of bone and muscle. Moreover, the analysis of fat composition showed a higher availability of essential fatty acids in the female sex than in their male counterparts and also in the Iberian genotype than in crossbred fetuses. These results are of high translational value for understanding ethnic differences in prenatal programming of postnatal health and disease status, and show evidence that prenatal development and metabolic traits are primarily determined by fetal sex and strongly modulated by fetal genotype.

Maternal quercetin intake during lactation attenuates renal inflammation and modulates autophagy flux in high-fructose-diet-fed female rat offspring exposed to maternal malnutrition

2019 ◽  
Vol 10 (8) ◽  
pp. 5018-5031 ◽  
Author(s):  
Shin Sato ◽  
Toshio Norikura ◽  
Yuuka Mukai
Keyword(s):  
Female Offspring ◽  
Female Rat ◽  
Autophagy Flux ◽  
Maternal Malnutrition ◽  
High Fructose Diet ◽  
Rat Offspring ◽  
Low Protein ◽  
High Fructose ◽  
Protein Diets

Quercetin intake during lactation causes long-term alterations in inflammation and autophagy flux in the kidneys of high-fructose-diet-fed adult female offspring exposed to maternal normal- or low-protein diets.

scholarly journals Digit length may reveal unusual breeding behaviour in a seabird

2008 ◽  
Vol 4 (5) ◽  
pp. 461-464 ◽  
Author(s):  
Meritxell Genovart ◽  
Maite Louzao ◽  
José M Igual ◽  
Daniel Oro
Keyword(s):  
Sexual Orientation ◽  
Cooperative Breeding ◽  
Prenatal Development ◽  
Cooperative Behaviour ◽  
Vertebrate Species ◽  
Wild Populations ◽  
Breeding Behaviour ◽  
Starting Point ◽  
Show Evidence ◽  
Digit Length

The hormonal environment experienced during prenatal development may affect adult phenotype and behaviour. Digit lengths may provide an estimate of steroid levels encountered during embryonic development in humans and other vertebrates. Finger patterns in humans have been shown to reveal sexual orientation or cooperative behaviour. We explored individual breeding behaviour in a monogamous seabird, the Balearic shearwater Puffinus mauretanicus and unexpectedly detected some cooperative breeders. Furthermore, we show evidence of correlation between digit lengths and cooperative breeding in this species. Additionally, we suggest that the first digit could be a possible indicator of prenatal steroid levels. These results are the starting point for further tests of the hypothesis that first digit length is an indicator of prenatal hormone levels in other vertebrate species. Moreover, these results may offer practical use in wild populations to study the implications of the changes in prenatal environment for adult social behaviour.

Influence of morphine during pregnancy on neuroendocrine regulation of pituitary hormone secretion

1983 ◽  
Vol 98 (2) ◽  
pp. 289-295 ◽  
Author(s):  
W. J. Litto ◽  
J. P. Griffin ◽  
Jamshid Rabii
Keyword(s):  
Hormone Secretion ◽  
Prenatal Development ◽  
Female Offspring ◽  
Morphine Sulphate ◽  
Pituitary Hormone ◽  
Critical Periods ◽  
Male And Female ◽  
Hypothalamic Pituitary Axis ◽  
Prolactin Response ◽  
Major Reduction

The effects of exposure to morphine during pregnancy on postnatal neuroendocrine systems were investigated. Rats received morphine sulphate or 0·9% (w/v) NaCl twice daily on days 5–12 of pregnancy. A dose of 5 mg morphine sulphate/kg was administered for the first three injections while 10 mg/kg was used for each of the remaining 13. This treatment regimen led to a significant delay in the onset of vaginal opening in the female offspring. Mothers treated with morphine sulphate showed a marked attenuation of their prolactin response to the suckling stimulus, although they still released significant amounts of the hormone. Both male and female offspring of the opiate-treated dams showed a major reduction in the sensitivity of their hypothalamic-pituitary axis to gonadal steroids at 15 days of age. No significant differences were found in the acute thyrotrophin response to single injection of morphine sulphate of prepuberal male and female pups of morphine- and saline-treated dams. These data show that exposure to opiates during critical periods of prenatal development lead to long-lasting alterations in the neuroendocrine control systems of the animal. These alterations may then have significant consequences on the physiological maturation and adult behaviour of the animal.

Intergenerational response of steroidogenesis-related genes to maternal malnutrition

2019 ◽  
Vol 10 (5) ◽  
pp. 587-594
Author(s):  
Abdel Halim Harrath ◽  
Abdulkarem Alrezaki ◽  
Saleh H. Alwasel ◽  
Abdelhabib Semlali
Keyword(s):  
Gene Expression ◽  
Reproductive Success ◽  
Adaptive Response ◽  
Food Restriction ◽  
Reproductive Capacity ◽  
Maternal Malnutrition ◽  
Pubertal Onset ◽  
Ovarian Aging ◽  
Premature Ovarian Aging ◽  
Predictive Adaptive Response

AbstractWe sought to examine whether rat maternal food restriction (MFR) affects the expression of steroidogenesis-related genes Cyp19, Cyp17a1, Insl3 and Gdf-9 in the ovaries of offspring from the first (FRG1) and second (FRG2) generations at pre-pubertal age (week 4) and during adulthood (week 8). At week 4, MFR significantly increased the expression of RNAs for all analyzed genes in both FRG1 and FRG2 females, which may indicate that MFR affects the onset of the reproductive lifespan, by inducing early pubertal onset. At week 8, the Cyp19 gene was still upregulated in MRF-subjected animals (Cyp19: P=0.0049 and P=0.0508 in FRG1 and FRG2, respectively), but MFR induced a significant decrease in Cyp17 and Gdf-9 gene expression in the offspring of both FRG1 and FRG2 females when compared with the controls (Cyp17: P=0.0018 and P=0.0016, respectively; Gdf-9: P=0.0047 and P=0.0023, respectively). This suggests that females at week 8, which should normally be in their optimal reproductive capacity, experience premature ovarian aging. At week 4, the activation of Cyp19 and Cyp17 was higher in the FRG1 ovaries than in the FRG2 ovaries, whereas the extent of Insl3 and Gdf-9 activation was lower in the FRG1 ovaries. This may indicate that FRG2 females were more vulnerable to MFR than their mothers (FRG1) and grandmothers, which is consistent with the ‘predictive adaptive response’ hypothesis. Our findings reveal that MFR may induce intergenerational ovarian changes as an adaptive response to ensure reproductive success before death.

scholarly journals Adult disease: echoes of the past

2006 ◽  
Vol 155 (suppl_1) ◽  
pp. S47-S50 ◽  
Author(s):  
P D Gluckman ◽  
M A Hanson
Keyword(s):  
Adaptive Response ◽  
Environmental Influence ◽  
Experimental Testing ◽  
Prenatal Development ◽  
Phenotypic Traits ◽  
Adaptive Responses ◽  
Adult Disease ◽  
Postnatal Environment ◽  
Predictive Adaptive Response ◽  
Environmental Challenge

Disease occurs if an environmental challenge exceeds the ability of an individual to mount an effective adaptive response to it. Evolution has selected genomically determined traits, which are optimal for a species to survive the historical environment. However, this adaptive ability to withstand an environmental challenge varies among individuals and is itself a phenotypic characteristic: how is this determined? We argue that maternal and placental cues that constrain prenatal development, induce offspring to develop predictive adaptive responses more suited to a deprived postnatal environment, i.e. a more favorable phenotype for survival of the species than that which would be established by the genotype in the absence of environmental influence. This ‘survival phenotype’ can be exaggerated further by the postnatal environment. Since predictive adaptive responses maximize the chance of survival to reproduce, this phenomenon has itself been protected through evolution. Furthermore, such rapid adaptive responses may allow transgenerational transmission of phenotypic traits advantageous for survival of a species through transient environmental change. We argue that risk of disease is increased, when the actual postnatal environment does not match that predicted prenatally. In humans, this explains patterns of disease, especially those for which risk is determined in part during development, such as type 2 diabetes, cardiovascular disease and the rising risks of childhood obesity. The predictive adaptive response hypothesis extends foregoing concepts in this field and lends itself to experimental testing. It provides insights into ways to reduce the burden of certain common chronic diseases in both developed and developing countries.

scholarly journals Comparative studies of placentation and immunology in non-human primates suggest a scenario for the evolution of deep trophoblast invasion and an explanation for human pregnancy disorders

Reproduction ◽  
2011 ◽  
Vol 141 (4) ◽  
pp. 391-396 ◽  
Author(s):  
Anthony M Carter
Keyword(s):  
Human Interaction ◽  
Trophoblast Invasion ◽  
Old World Monkeys ◽  
Reproductive Disorders ◽  
Old World ◽  
Human Pregnancy ◽  
Uterine Natural Killer Cells ◽  
Maternal Genotype ◽  
Increased Risk ◽  
Fetal Genotype

Deep trophoblast invasion in the placental bed has been considered the hallmark of human pregnancy. It occurs by two routes, interstitial and endovascular, and results in transformation of the walls of the spiral arteries as they traverse the decidua and the inner third of the myometrium. Disturbances in this process are associated with reproductive disorders such preeclampsia. In contrast, trophoblast invasion in Old World monkeys occurs only by the endovascular route and seldom reaches the myometrium. Recently, it was shown that this pattern is maintained in gibbons, but that the human arrangement also occurs in chimpanzee and gorilla. There is an interesting parallel with results from placental immunology regarding the evolution of the major histocompatability complex class I antigen HLA-C and its cognate receptors. HLA-C is not present in Old World monkeys or gibbons. It emerged in the orangutan and became polymorphic in the lineage leading to gorilla, bonobo, chimpanzee, and human. Interaction between HLA-C1 and HLA-C2 on the surface of trophoblast and killer immunoglobulin-like receptors (KIRs) expressed by uterine natural killer cells are important regulators of trophoblast invasion. Evolution of this system in great apes may have been one prerequisite for deep trophoblast invasion but seems to have come at a price. The evidence now suggests that certain combinations of maternal genotype for KIRs and fetal genotype for HLA-C imply an increased risk of preeclampsia, fetal growth restriction, and recurrent abortion. The fetal genotype is in part derived from the father providing an explanation for the paternal contribution to reproductive disorders.

526. GENETIC POLYMORPHISMS IN INTERLEUKIN-1 FAMILY MEMBERS AND PREGNANCY OUTCOME

2009 ◽  
Vol 21 (9) ◽  
pp. 125
Author(s):  
R. C. Nowak ◽  
S. D. Thompson ◽  
J. Zhang ◽  
G. A. Dekker ◽  
C. T. Roberts
Keyword(s):  
Pregnancy Outcome ◽  
Head Circumference ◽  
Interleukin 1 ◽  
Competitive Inhibitor ◽  
Placental Weight ◽  
Trophoblast Invasion ◽  
Placental Development ◽  
Maternal Genotype ◽  
And Function ◽  
Fetal Genotype

Poor placental development is associated with a variety of common, potentially life-threatening pregnancy complications, including preeclampsia (PE) and small-for-gestational-age (SGA) babies. The placenta and fetus express a combination of maternal and paternal genes. Interleukin-1 alpha (IL-1α) and -1 beta (IL-1β) promote trophoblast invasion by upregulating expression of matrix metalloproteinases, while interleukin-1 receptor antagonist (IL-1RN) acts as a competitive inhibitor of IL-1 a and IL-1β by binding to the IL-1 receptor. We hypothesis that polymorphisms which decrease IL-1 activity, within IL-1α rs1800587 (C-allele) and rs17561 (T-allele), IL-1β rs16944 (C-allele) and IL-1RN rs454078 (A-allele) affect placental development and thus pregnancy outcome. To determine the effect of the IL-1 SNPs on pregnancy outcome, blood was collected prospectively from pregnant women at 15 weeks gestation and from their partners and babies at birth. DNA was extracted and genotyped by Sequenom MassArray. Pregnancies were fully characterised and classified into control or PE, PE+SGA, SGA after delivery by an experienced obstetrician. The IL-1α rs1800587 fetal genotype was associated with PE+SGA and smaller head circumference at birth. IL-1α rs17561 fetal genotype was associated with PE+SGA, and a smaller head circumference and body length at birth. The frequency of IL-1β C-allele was associated with PE in neonates, and in fathers the CC homozygote genotype was associated with decreased placental weight at birth. The IL-1RN rs454078 maternal genotype was associated with PE and maternal waist circumference while fetal AA genotype was associated with SGA and decreased placental weight at birth. Genotypes which decrease the production of IL-1α and IL-1β while increasing IL-1RN will reduce proinflammatory cytokines and thereby affect the invasive potential of placental trophoblasts. We have shown that these polymorphisms in both parents may be associated with poor pregnancy outcome. Suggesting that both partners contribute to placental differentiation and function.

Radionuclide Bone Scan in Neuroblastoma

PEDIATRICS ◽  
1983 ◽  
Vol 71 (2) ◽  
pp. 206-209
Author(s):  
Margaret A. Heisel ◽  
John H. Miller ◽  
Barbara S. Reid ◽  
Stuart E. Siegel
Keyword(s):  
Physical Examination ◽  
Metastatic Disease ◽  
Primary Tumor ◽  
Bone Scan ◽  
Disease Status ◽  
Show Evidence ◽  
Bone Scans

A comparison of radionuclide bone scans with other methods of monitoring disease status was undertaken in a series of 51 children with neuroblastoma. The radionuclide bone scan was more accurate than either conventional radiographic studies or physical examination in localizing the primary tumor. When the extent of bony metastatic disease was evaluated, the bone scan and radiographic skeletal surveys were generally both positive, but the bone scan tended to show evidence of greater metastatic disease than radiographs.

Comparative reproductive performance in Meishan and Large White pigs and their crosses

1995 ◽  
Vol 60 (2) ◽  
pp. 259-267 ◽  
Author(s):  
C. S. Haley ◽  
G. J. Lee ◽  
M. Ritchie
Keyword(s):  
Litter Size ◽  
Weighted Average ◽  
Additive Effect ◽  
Ovulation Rate ◽  
White Female ◽  
Large White ◽  
Gene Effects ◽  
Genetic Components ◽  
Breed Difference ◽  
Maternal Genotype

AbstractA crossbreeding trial extending over three generations was used to investigate the genetic components contributing to the prolificacy of the Meishan breed in comparison with the Large White breed. Information on the number of teats and on body weight and litter size in the first two parities was recorded on purebred Meishan and Large White females and on reciprocal F1 and backcross females. Ovulation rate was also recorded for all litters, allowing the estimation of per litter prenatal survival. Crossbreeding parameters for direct, maternal and grandmaternal effects were estimated using restricted maximum likelihood analysis. There was a consistent advantage of three to four piglets born alive to the Meishan female compared with the Large White female. This was controlled by the maternal genotype, with no effect of the genotype of the litter itself. Both additive and heterosis effects were important, the contribution of additive maternal effects to the breed difference being similar across parities (4·0 (s.e. 1·1) and 4·2(s.e. 1·1), in the two parities respectively) and the maternal heterosis increasing slightly across parities (2·2 (s.e. 0·8) and 2·9 (s.e. 0·8), in the two parities respectively). The number born alive to F 1 females was similar to, or greater than, the number born alive to Meishan females. Ovulation rate was significantly higher in Meishan than in Large White females and this was controlled by additive gene effects which had a similar effect across parities, the weighted average of their contribution to the breed difference being 5·7 (s.e. 0·8) ova. Differences between the breeds in prenatal survival were small, although there was significant maternal heterosis, however, the maternal additive effect became significant after the inclusion of ovulation rate as a covariate. After adjustment for ovulation rate, the weighted average estimates across parity of the maternal additive contribution to the breed difference and the maternal heterosis for the proportional prenatal survival loere 0-14 (s.e. 0·05) and 0·13 (s.e. 0·03), respectively. This suggests that a combination of a high ovulation rate and especially a high level of prenatal survival for that ovulation rate led to the prolificacy observed in this sample of Meishan pigs. The inclusion of ovulation rate as a covariate in the analysis of number born alive confirms this view, as the maternal additive effect on litter size was only reduced by about one third and the heterosis effect was largely unchanged. Both numbers stillborn and mummified were increased in litters born to Meishan sows due to maternal additive effects, but the effects seemed largely a consequence of the increased ovulation rate as they became non-significant after its inclusion as a covariate in the model.

The Cellular Origin in Atheromatous Lesion

1970 ◽  
Vol 28 ◽  
pp. 202-203
Author(s):  
T. M. Murad ◽  
H. A. I. Newman ◽  
K. F. Kern
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Rabbit Aorta ◽  
Mixed Population ◽  
The Other ◽  
Cellular Origin ◽  
Ultrastructural Studies ◽  
Atherosclerotic Lesions ◽  
Show Evidence ◽  
Early Lesion

The origin of lipid containing cells in atheromatous lesion has been disputed. Geer in his study on atheromatous lesions of rabbit aorta, suggested that the early lesion is composed mainly of lipid-laden macrophages and the later lesion has a mixed population of macrophages and smooth muscle cells. Parker on the other hand, was able to show evidence that the rabbit lesion is primarily composed of lipid-laden cells of smooth muscle origin. The above studies and many others were done on an intact lesion without any attempt of cellular isolation previous to their ultrastructural studies. Cell isolation procedures have been established for atherosclerotic lesions through collagenase and elastase digestion Therefore this procedure can be utilized to identify the cells involved in rabbit atheroma.

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