scholarly journals Maternal Undernutrition during Late Gestation Induces Fetal Overexposure to Glucocorticoids and Intrauterine Growth Retardation, and Disturbs the Hypothalamo-Pituitary Adrenal Axis in the Newborn Rat1

Endocrinology ◽  
2001 ◽  
Vol 142 (5) ◽  
pp. 1692-1702 ◽  
Author(s):  
J. Lesage ◽  
B. Blondeau ◽  
M. Grino ◽  
B. Bréant ◽  
J. P. Dupouy
Keyword(s):  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Late Gestation ◽  
Intrauterine Growth ◽  
Maternal Undernutrition ◽  
Adrenal Axis ◽  
Pituitary Adrenal Axis

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.

A model of intrauterine growth retardation caused by chronic maternal undernutrition in the rat: effects on the somatotrophic axis and postnatal growth

1996 ◽  
Vol 150 (2) ◽  
pp. 231-242 ◽  
Author(s):  
S M Woodall ◽  
B H Breier ◽  
B M Johnston ◽  
P D Gluckman
Keyword(s):  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Postnatal Growth ◽  
Maternal Plasma ◽  
Intrauterine Growth ◽  
Maternal Undernutrition ◽  
Body Weights ◽  
Igf I ◽  
Ad Libitum ◽  
Somatotrophic Axis

Abstract While it is well established that severe maternal undernutrition during pregnancy causes intrauterine growth retardation (IUGR), there has been relatively little study of the endocrine consequences and postnatal development of growth-retarded offspring. We have developed a model in the rat of IUGR by nutritional restriction of the mother throughout gestation and have examined the effects of fetal growth retardation on the endocrine and metabolic status during the perinatal period. Timed matings were performed in Wistar rats and dams were randomly assigned to one of two dietary treatment groups. Food was available ad libitum throughout pregnancy to a control group (ad libitum group) and a restricted group was fed 30% of the ad libitum intake (restricted fed group). After birth, food was available ad libitum in both groups and litter size was adjusted to eight pups per litter. Dams lost a significant amount of body weight throughout gestation due to undernutrition but were able to catch up to the ad libitum group by day 10 postnatally. Litter size was not affected by maternal undernutrition. Maternal plasma IGF-I levels were significantly reduced in the restricted fed group throughout gestation (P<0·001) but were not different postnatally. Maternal plasma IGF-binding proteins (IGFBPs)-1, -2 and -3 were significantly (P<0·05) increased in the restricted fed dams. The mean body weights of fetuses in late gestation from the restricted fed dams were significantly lower (P<0·001) in comparison with fetuses from control dams. Placental weights were also significantly (P<0·01) reduced in the restricted fed compared with control dams. Body weights were significantly lower in the offspring of restricted fed dams than control dams from birth (P<0·01) until 90 days of age (P<0·05). Nose–rump length was reduced in the fetuses of the restricted fed group at day 22 of gestation (P<0·001) until weaning (P<0·05). Plasma IGF-I levels were significantly reduced in the pups of restricted fed dams from day 22 of gestation (P<0·01) until postnatal day 9 (P<0·05) but were not significantly different at the later time-points. Plasma insulin levels were significantly reduced in the pups of restricted fed dams at birth (P<0·05) but not at later time-points. Plasma IGFBP-1 and -2 levels were significantly increased in the offspring from restricted fed dams at day 22 of gestation, at birth and at day 9 postnatally (P<0·05). 125I-Bovine GH specific binding to liver membranes was significantly lower (P<0·05) in offspring from restricted fed dams at 21 days of age but not at 90 days of age. These data demonstrate that nutritional deprivation in the pregnant rat leads to IUGR and postnatal growth failure and to changes in allometric growth patterns and endocrine parameters of the somatotrophic axis postnatally. Journal of Endocrinology (1996) 150, 231–242

Influences on fetal and placental weights during mid to late gestation in prolific ewes well nourished throughout pregnancy

2000 ◽  
Vol 12 (4) ◽  
pp. 149 ◽  
Author(s):  
Paul L. Greenwood ◽  
Ramona M. Slepetis ◽  
Alan W. Bell
Keyword(s):  
Litter Size ◽  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Placental Weight ◽  
Late Gestation ◽  
Fetal Weight ◽  
Intrauterine Growth ◽  
Weight Variation ◽  
Condition Score ◽  
Tightly Coupled

This study investigated associations between fetal and placental weights from 85 to 130 days gestation in 49 fetuses from 21 ewes of a prolific genotype used as an experimental model of intrauterine growth retardation. The proportion of variation in fetal weight explained by placental weight increased from zero at 85 days to 91% (residual standard deviation (RSD) = 260 g) at 130 days. Overall, stage of pregnancy plus placental weight accounted for 96% of fetal weight variation (RSD = 212 g). Litter size and number of fetuses per uterine horn also influnced individual fetal weights. Gestational age, litter size, placental weight per ewe, and liveweight and condition score of ewes during early to mid gestation (initial LW and CS) explained 99.5% of the variation in fetal weight per ewe (RSD = 236 g). Most variation (86%) in placental weight was explained by stage of pregnancy, litter size, number of placentomes, and initial LW and CS (RSD = 53 g). Placental weight per ewe was influenced by stage of pregancy, litter size and initial ewe LW and CS (R 2 = 0.97; RSD = 89 g). The association of fetal and placental weights with initial ewe LW was positive, and with initial CS was negative. The results show that in the absence of overt nutritional restriction of pregnant ewes, fetal and placental weights are tightly coupled during late gestation and ewe fatness during early pregnancy is inversely related to placental and fetal weights. They demonstrate that placental weight explains most of the variation in fetal weight in the present intrauterine growth retardation model.

Molecular approach to intrauterine growth retardation: an overview of recent data

1995 ◽  
Vol 7 (6) ◽  
pp. 1457 ◽  
Author(s):  
E Alsat ◽  
C Marcotty ◽  
R Gabriel ◽  
A Igout ◽  
F Frankenne ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Molecular Mechanisms ◽  
Late Gestation ◽  
Placental Development ◽  
Intrauterine Growth ◽  
Placental Growth Hormone

Consideration of the abnormal regulation of fetal growth leading to intrauterine growth retardation must take account of the fundamental differences between the regulation of growth before and after birth. The significance of endocrine regulators of growth differs greatly in utero. During the first trimester of pregnancy, embryonic growth might be controlled at the level of the individual organs by nutrient supply and by locally active growth factors. Later, fetal growth depends essentially upon materno-placental cooperation in delivering nutrients to the fetus. Therefore the major role of hormones in fetal growth is to mediate utilization of available substrate. Fetal growth seems to be regulated by fetal insulin, IGF-1 and certainly IGF-2, while growth hormone has only a secondary role to play. In late gestation, placental size and fetal growth rate are well correlated, pointing to a key role of the placenta in the regulation of fetal growth. It is therefore of importance to understand the molecular mechanisms involved in regulating placental development and endocrine functions. TGF alpha and EGF might play a major role as suggested by the modulation of their receptors with placental development, and by the specific alterations of epidermal growth factor receptors in intrauterine growth retardation. In addition, human placenta secretes specifically placental growth hormone. The concentration of placental growth hormone is significantly decreased in sera of pregnant women bearing a fetus with intrauterine growth retardation.

Imbalance in the system L-arginin-NO in pathogenesis of obstetric complications and intrauterine growth retardation (Literature review)

2016 ◽  
pp. 43-47
Author(s):  
O.V. Basystyi ◽  
Keyword(s):  
Nitric Oxide ◽  
Literature Review ◽  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Obstetric Complications ◽  
Pathogenetic Role ◽  
Intrauterine Growth ◽  
System L ◽  
Nitric Oxide Deficiency

The data of domestic and foreign literature on etiology, pathogenesis and intrauterine growth retardation diagnosis are presented in the paper. It highlights pathogenetic role of nitric oxide deficiency in case of obstetric complications and intrauterine growth retardation. Key words: intrauterine growth retardation (IUGR), system L-arginin–NO, obstetric complications.

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