Effect Of Prenatal Protein Deprivation Research Articles

Reduced protein availability by albumen removal during chicken embryogenesis decreases body weight and induces hormonal changes.

What is the central question of this study? Prenatal protein undernutrition by albumen removal in an avian model of fetal programming leads to long-term programming effects, but when do these effects first appear and are these programming effects regulated by the same candidate genes as in mammals? What is the main finding and its importance? The present results indicate that prenatal protein undernutrition by albumen removal induces phenotypical and hormonal changes in the early posthatch period, when the mismatch between the prenatal and postnatal environment first arises, but these changes are not accompanied by an altered gene expression of the selected candidate genes. Studies of the chicken offer a unique model for investigation of the direct effects of reduced prenatal protein availability by the partial replacement of albumen with saline in eggs at embryonic day1 (albumen-deprived group). The results were compared with mock-treated sham chicks and non-treated control chicks. Although no differences in hatch weight were found, body weight and growth were reduced in the albumen-deprived chicks until 3weeks of age. The feed intake of the albumen-deprived chicks, however, was increased compared with the control (day13-21) and the sham chicks (day16-18). In the albumen-deprived chicks, the ratio of thyroxine to 3,5,3'-triiodothyronine in the plasma was increased compared with the control chicks, whereas the plasma corticosterone level was increased only at day 7 compared with both other groups. The plasma glucose concentration and glucose tolerance were not affected by treatment. Several candidate genes previously associated with effects of prenatal protein deprivation in mammals were examined in the liver of newly hatched chicks. Gene expression of glycogen synthase2, glycogen phosphorylase1, peroxisome proliferator-activated receptor α and γ and glucocorticoid receptor was not affected by the treatment. In conclusion, reduction of prenatal protein availability led to differences in body weight and influenced hormones involved in metabolism and growth. Gene expression of the selected candidate genes was not altered, in contrast to mammals.

Prenatal protein deprivation alters dopamine-mediated behaviors and dopaminergic and glutamatergic receptor binding

Epidemiological evidence indicates that prenatal nutritional deprivation may increase the risk of schizophrenia. The goal of these studies was to use an animal model to examine the effects of prenatal protein deprivation on behaviors and receptor binding with relevance to schizophrenia. We report that prenatally protein deprived (PD) female rats showed an increased stereotypic response to apomorphine and an increased locomotor response to amphetamine in adulthood. These differences were not observed during puberty. No changes in haloperidol-induced catalepsy or MK-801-induced locomotion were seen following PD. In addition, PD female rats showed increased 3H-MK-801 binding in the striatum and hippocampus, but not in the cortex. PD female rats also showed increased 3H-haloperidol binding and decreased dopamine transporter binding in striatum. No statistically significant changes in behavior or receptor binding were found in PD males with the exception of increased 3H-MK-801 binding in cortex. This animal model may be useful to explore the mechanisms by which prenatal nutritional deficiency enhances risk for schizophrenia in humans and may also have implications for developmental processes leading to differential sensitivity to drugs of abuse.

Birthdates and Number of Neurons in the Serotonergic Raphe Nuclei in the Rat with Prenatal Protein Malnutrition

The effect of prenatal protein deprivation on timing of neurogenesis and on number of neurons generated in the serotonergic dorsal (DR) and median raphe (MR) nuclei of the rat was studied. These neurons are of interest because their neurogenesis occurs during the period of malnutrition and their axonal projections participate in the earliest stages of brain development. In this study, dams were maintained on a 25% casein diet or a 6% casein diet 5 weeks prior to mating and throughout pregnancy. At birth, all pups were cross-fostered to dams on a 25% casein diet. Bromodeoxyuridine, a thymidine analog that is incorporated into nuclear deoxyribonucleic acid during the cell cycle synthetic phase, was used as a marker of neurogenesis. Bromodeoxyuridine was administered on either embryonic day 11, 12, 13 or 14. On postnatal day 30, serial sections of raphe nuclei were processed with bromodeoxyuridine immunocytochemistry to determine the number of raphe cells generated on each day and with Nissl stain to determine the total number of cells generated. There were no significant differences between the two diet groups in timing of generation or in total number of cells generated, indicating that neurogenesis of these early generated neurons appears unaffected by concomitant protein deprivation.

Effects of prenatal protein malnutrition on mossy fibers of the hippocampal formation in rats of four age groups.

The present study was undertaken to investigate the effect of prenatal protein deprivation on the postnatal development of the mossy fiber plexus of the hippocampal formation on postnatal (P) days 15, 30, 90, and 220. Although there is extensive information about the effects of malnutrition on cell body and dendrite morphology, little attention has been paid to axons or axon plexuses. The mossy fiber plexus represents the dentate gyrus granule cell axonal projection to areas CA4 and CA3 of the hippocampal formation and is readily demonstrated with Timm's heavy metal stain. With the use of this stain, the plexus was measured at 13 levels throughout the hippocampal complex. There was no effect of the diet on the anatomical distribution of the plexus. The current study, however, does show significant effects of prenatal protein malnutrition on postnatal development of the mossy fiber plexus that are age dependent. The prenatally malnourished rats show significant deficits in the total rostro-caudal extent and volume of the plexus on P15, P90, and P220, with the most marked dietary effect on P220. There was no significant diet effect on P30 in either extent or volume.

Effects of prenatal protein malnutrition on hippocampal CA1 pyramidal cells in rats of four age groups

The present study was undertaken to investigate the effect of prenatal protein deprivation on area CA1 hippocampal pyramidal cells on postnatal (P) days 15, 30, 90 and 220 using Golgi techniques. Age related changes in both groups and diet related changes between groups were assessed. There were significant diet effects at all four ages, with one of 12 different measurements showing a significant diet effect on P15, five on P30, one on P90, and seven on P220. The most marked effect of the diet was on pyramidal cell dendrite spine density in the stratum moleculare and stratum radiatum, with a different pattern of diet effects in the two strata. In pyramidal cell dendrites in the stratum moleculare, there was a deficit in spine density that was significant at three of the four ages and there were similar age-related changes in the two diet groups. Spines on pyramidal cell dendrites in the stratum radiatum showed a lack of synchrony of age-related changes in the two diet groups, with an increased spine density in the malnourished rats on P30 and a widening deficit in this parameter on P90 and P220. The bimodal distribution to these changes, with most marked deficits occurring on P30 and P220, with an intervening period of apparent “catch-up” on P90, is of interest and may be a significant brain adaptation to malnutrition. The present study is the final of three morphometric studies on the effect of prenatal protein restriction on three key neurons in the hippocampal trisynaptic circuit. When compared to our previous studies on the dentate granule cell and the CA3 pyramidal cell, it is noted that there is an effect of the low protein diet on all these neurons, with the most marked effect on the predominantly postnatally generated dentate granule cells. Hippocampus 7:192–203, 1997. © 1997 Wiley-Liss, Inc.

Effects of prenatal protein malnutrition on mossy fibers of the hippocampal formation in rats of four age groups

The present study was undertaken to investigate the effect of prenatal protein deprivation on the postnatal development of the mossy fiber plexus of the hippocampal formation on postnatal (P) days 15, 30, 90, and 220. Although there is extensive information about the effects of malnutrition on cell body and dendrite morphology, little attention has been paid to axons or axon plexuses. The mossy fiber plexus represents the dentate gyrus granule cell axonal projection to areas CA4 and CA3 of the hippocampal formation and is readily demonstrated with Timm's heavy metal stain. With the use of this stain, the plexus was measured at 13 levels throughout the hippocampal complex. There was no effect of the diet on the anatomical distribution of the plexus. The current study, however, does show significant effects of prenatal protein malnutrition on postnatal development of the mossy fiber plexus that are age dependent. The prenatally malnourished rats show significant deficits in the total rostro-caudal extent and volume of the plexus on P15, P90, and P220, with the most marked dietary effect on P220. There was no significant diet effect on P30 in either extent or volume. Hippocampus 7:184–191, 1997. © 1997 Wiley-Liss, Inc.

Effects of prenatal protein malnutrition on hippocampal CA1 pyramidal cells in rats of four age groups.

The present study was undertaken to investigate the effect of prenatal protein deprivation on area CA1 hippocampal pyramidal cells on postnatal (P) days 15, 30, 90 and 220 using Golgi techniques. Age related changes in both groups and diet related changes between groups were assessed. There were significant diet effects at all four ages, with one of 12 different measurements showing a significant diet effect on P15, five on P30, one on P90, and seven on P220. The most marked effect of the diet was on pyramidal cell dendrite spine density in the stratum moleculare and stratum radiatum, with a different pattern of diet effects in the two strata. In pyramidal cell dendrites in the stratum moleculare, there was a deficit in spine density that was significant at three of the four ages and there were similar age-related changes in the two diet groups. Spines on pyramidal cell dendrites in the stratum radiatum showed a lack of synchrony of age-related changes in the two diet groups, with an increased spine density in the malnourished rats on P30 and a widening deficit in this parameter on P90 and P220. The bimodal distribution to these changes, with most marked deficits occurring on P30 and P220, with an intervening period of apparent "catch-up" on P90, is of interest and may be a significant brain adaptation to malnutrition. The present study is the final of three morphometric studies on the effect of prenatal protein restriction on three key neurons in the hippocampal trisynaptic circuit. When compared to our previous studies on the dentate granule cell and the CA3 pyramidal cell, it is noted that there is an effect of the low protein diet on all these neurons, with the most marked effect on the predominantly postnatally generated dentate granule cells.

Effect of prenatal protein deprivation on postnatal granule cell generation in the hippocampal dentate gyrus.

The effect of prenatal malnutrition, produced by protein deprivation, on postnatal neurogenesis of granule cells in the fascia dentata of the rat hippocampal formation was examined by injecting tritiated thymidine on P8 and P15 and sacrificing the pups on P30, or by injecting on P30 and sacrificing on P90. The number of labeled granule cells was significantly decreased in prenatally malnourished rats injected on P8, and unaffected in those injected on P15. In contrast, the number of labeled granule cells in prenatally malnourished rats was significantly increased in animals injected in P30. The study shows that prenatal malnutrition significantly alters the postnatal pattern of granule cell neurogenesis in rat hippocampal formation and that the effect persists despite nutritional rehabilitation at birth.

Effects of prenatal protein deprivation on postnatal development of granule cells in the fascia dentata

The effect of prenatal protein deprivation on the postnatal development of granule cells in the fascia dentata in the rat was studied at 15, 30, 90, and 220 days of age. The granule cells showed a significant reduction in cell size, decreased number of synaptic spines throughout their dendritic extent, and reduced complexity of dendritic branching in the outer two-thirds of the molecular layer. All of these deficits were present at 15 days and persisted throughout the study (220 days). The least deficits in synaptic spine density occurred at 90 days and in dendritic branching at 30 days. Partial restitution of earlier, more severe deficits was associated primarily with maturational events occurring in the protein deprived rats, whereas later increases in deficits were related primarily to a failure of the protein deprived rats to keep pace with neuronal development occurring in the controls. The present results are similar to those noted in our previous study in this journal of the effect of a low protein diet (8% casein) on these neurons that extended from pregnancy until the time of sacrifice at 30, 90, and 220 days of age (Cintra et al., '90; 532:271-277). Taken together, these two studies suggest that the postnatal adaptation of the granule cells to prenatal protein deprivation is primarily due to events that occur during pregnancy and that the site of predilection for the deficit is their dendrites in the outer two-thirds of the molecular layer of the fascia dentata.

The Effects of Maternal Protein Deprivation on Renal Development and Function in Neonatal Rats

This study was undertaken to investigate the effects of pre- and/or postnatal maternal protein deprivation (PD) on renal functional development in the offspring. Pregnant rats were fed either a control (24% protein) or low (8 or 10%) protein diet during gestation and lactation. Progeny of these dams were cross-fostered at birth, yielding four experimental groups: pups born of control dams and nursed by PD or control dams and pups born of PD dams and nursed by control or PD dams. While the effects of prenatal PD on body and kidney growth were negligible, PD during the nursing period appeared to have a more profound effect on body and kidney weight. Renal transport functions, quantified in vitro, were differentially affected by these dietary manipulations. Renal transport capacity for organic acids and bases was depressed in pups nursed by PD dams. Maturation of the renal organic acid transport system was also delayed in these pups. alpha-Aminoisobutyric acid accumulation by renal cortical slices was enhanced only in 10-day old rats stressed by pre- and postnatal maternal PD. Renal gluconeogenic and ammoniagenic capacity was not impaired by these dietary manipulations. No differences in protein or water content of renal cortical slices were observed.

Effect of Prenatal Protein Deprivation on Fetal and Neonatal Thyroid Morphology in the Rat

Morphogenesis of the thyroid was compared in young of control and protein-deprived rats from day 17 of gestation through the first postpartum day. Examination of histological sections revealed a significant delay in follicle formation and a reduction in gland area, follicle number, colloid space and cell size in the thyroid tissue of fetal and neonatal pups of protein-deprived dams.

Effect of Prenatal Protein Deprivation on Dental Development in the Rat

Effect of Prenatal Protein Deprivation on Dental Development in the Rat

Effect of Pre-natal Protein Deprivation on Neonatal Cerebellar Development in vitro

MOST biochemical and morphological studies of the effects of nutritional deprivation on the mammalian nervous system have dealt with quantitative undernutrition during the first 21 postnatal days. Findings have included a reduction in brain cellularity1–4; a delay in neuronal and glial differentiation3; and a decrease in the lipids3,3–7, lamellae numbers8 and stainability3,5,9 of the myelin sheath. Such studies, even of those regions of the nervous system developing maximally post-natally, may be criticized as enabling the anlage, however undifferentiated, to develop normally until birth. I have, therefore, studied in a tissue culture system the morphogenetic effects of pre-natal maternal protein deprivation on the growth and development of the cerebellum, a region of the brain developing maximally after birth. Cultures of neonatal mouse cerebellum from mothers deprived of protein were analysed in a nutritionally normal environment to determine the effect of pre-natal protein restriction on the post-natal developmental potential of the nervous system.