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C Antipatis

Publications and source records attributed to C Antipatis.

12 recordsLinked to original sources
PubMed2004

Moderate maternal vitamin A deficiency alters myogenic regulatory protein expression and perinatal organ growth in the rat.

Vitamin A deficiency is one of the most common dietary deficiencies in the developing world and is a major health concern where it is associated with increased risk of fetal and infant mortality and morbidity. Early studies in the rat demonstrated that, in addition to respiratory problems, neonates showed evidence of mobility problems in response to moderate vitamin A deficiency. This study investigated whether moderate deficiency of this vitamin plays a role in regulating key skeletal muscle regulatory pathways during development. Thirty female rats were fed vitamin A-moderate (VAM) or vitamin A-sufficient diets from weaning and throughout pregnancy. Fetal and neonatal hindlimb and muscle samples were collected on days 13.5, 15.5, 17.5, and 19.5 of pregnancy and 1 day following birth. Mothers fed the VAM diet had reduced retinol concentrations at all time points studied (P < 0.01), and neonates had reduced relative lung weights (P < 0.01). Fetal weight and survival did not differ between groups but neonatal survival was lower in the VAM group where neonates had increased relative heart weights (P < 0.05). Analysis of myogenic regulatory factor expression and calcineurin signaling in fetuses and neonates demonstrated decreased protein levels of myf5 [50% at 17.5 dg (P < 0.05)], myogenin [70% at birth (P < 0.001)], and myosin heavy chain fast [50% at birth (P < 0.05)] in response to moderate vitamin A deficiency. Overall, these changes suggest that vitamin A status during pregnancy may have important implications for fetal muscle development and subsequent muscle function in the offspring.

Animals↗
PubMed2002

Patterns of fetal growth within Large White x Landrace and Chinese Meishan gilt litters at three stages of gestation.

Low birthweight piglets have an increased incidence of mortality and morbidity. As there are few opportunities to remedy the detrimental consequences of low birthweight after birth, it is important to understand the nature of fetal growth retardation and to identify when low birthweight fetuses deviate from the growth trajectory of their normally grown siblings. The aims of this study were to identify the nature, timing and possible causal factors influencing inadequate fetal growth in Large White x Landrace (LW) and Chinese Meishan (MS) gilts at three stages of pregnancy. Thirty-six per cent of litters contained inadequately grown fetuses. Both intrauterine-growth-restricted (IUGR) and small-for-gestational-age (SGA) fetuses could be identified as early as Day 30 in MS and LW litters and the percentage of litters containing inadequately grown fetuses was similar throughout gestation. MS fetuses, placentas and piglets had less within-litter variation in weight at all stages studied. Inverse relationships were observed between litter size and both minimum and mean weights of MS neonates. No other relationships between fetal size and either uterine position or litter size were observed.

Animals↗
PubMed2001

Micronutrient programming of development throughout gestation.

Vitamins and minerals serve essential roles in cellular metabolism, maintenance and growth throughout life. They are also central components of many enzymes and transcription factors. However, the need for optimum amounts of key micronutrients at critical stages during the periovulatory period and subsequent embryonic and fetal life has become the focus of sustained research activity only recently. In addition to folic acid, the minerals zinc, iron and copper and the antioxidant vitamins A and E are of particular importance during pregnancy. Both excesses and deficiencies of these micronutrients can have profound and sometimes persistent effects on many fetal tissues and organs in the absence of clinical signs of deficiency in the mother. The consequences of micronutrient imbalance on the developing conceptus may not be apparent at the time of the nutritional insult, but may be manifest later in development. However, supplementary micronutrients provided later in gestation or during postnatal life cannot completely reverse the detrimental effects of earlier micronutrient imbalance. Importantly, deficiency of a specific micronutrient, such as zinc, during pregnancy can result in a greater incidence of fetal malformation and resorptions than general undernutrition. Given the range of micronutrients that affect development, the number of developmental stages susceptible to inappropriate micronutrient status and the diverse biochemical systems and types of tissue affected, it is challenging to propose a unifying hypothesis that could explain the effects of micronutrient imbalance on programming throughout gestation. Micronutrient imbalance can affect pregnancy outcome through alterations in maternal and conceptus metabolism, as a consequence of their essential role in enzymes and transcription factors and through their involvement in signal transduction pathways that regulate development. Micronutrient-induced disturbances in the balance between the generation of free oxygen radicals and the production of antioxidants that scavenge free radicals may provide an additional mechanistic explanation. The detrimental effects of many micronutrient deficiencies, particularly zinc and copper, can be alleviated by supplementary antioxidants, whereas deficiencies of antioxidant vitamins A and E are likely to reduce defence against free radical damage.

Animals↗
PubMed2000

Maternal protein deficiency causes hypermethylation of DNA in the livers of rat fetuses.

Maternal protein deficiency during pregnancy is associated with changes in glucose tolerance and hypertension in the offspring of rats. In this study the growth of rat fetuses was examined when the dams were fed diets containing 18% casein, 9% casein or 8% casein supplemented with threonine. The extra threonine was added to reverse the decrease in circulating threonine concentrations that occurs when pregnant rats are fed protein-deficient diets. The fetuses of the group fed the low protein diet supplemented with threonine were significantly smaller than those of the control group and not significantly different from those fed low protein. Homogenates prepared from the livers of dams fed the diet containing 9% casein oxidized threonine at approximately twice the rate of homogenates prepared from dams fed the diet containing 18% casein. We conclude that circulating levels of threonine fall as a consequence of an increase in the activity of the pathway that metabolizes homocysteine produced by the transulfuration of methionine. Serum homocysteine was unaffected in the dams fed low protein diets compared with controls, but was significantly greater in dams fed the low protein diet supplemented with threonine. Elevated levels of homocysteine are associated with changes in the methylation of DNA. The endogenous methylation of DNA was greater than that of controls in the livers of fetuses from dams fed the 9% protein diets and increased further when the diet was supplemented with threonine. Our results suggest that changes in methionine metabolism increase homocysteine production, which leads to changes in DNA methylation in the fetus. An increase in maternal homocysteine may compromise fetal development, leading to the onset of glucose intolerance and hypertension in adult life.

Animals↗
PubMed2000

Moderate maternal vitamin A deficiency affects perinatal organ growth and development in rats.

Vitamin A deficiency during pregnancy is associated with detrimental effects in the offspring. We have developed a rat model to examine specific effects of maternal vitamin A status on perinatal growth and development. A total of 54 female rats were fed a vitamin A-free (VAF), -marginal (VAM) or -sufficient (VAS) diet from weaning until mating (at 7 weeks) and throughout pregnancy. Half of the rats in each group were injected with a single large dose of vitamin A on day 10 of pregnancy. Fetal and neonatal samples were taken on day 20 of pregnancy and the day of birth respectively. Maternal plasma retinol concentrations on day 20 and at birth were 50% and 30% lower in the VAF and VAM when compared to the VAS group. Fetal weight and survival did not differ between groups although placental:fetal ratio was higher in the VAF group than in the VAS group (0.195 (SE 0.005) v. 0.175 (SE 0.004), P < 0.05). Rats fed the VAF diet gave birth at 23.5 d, an average of 1 d later than the other groups, and had lower number of live neonates at birth. Fetal liver, heart and lung weights relative to total body weight were lower in the VAF group and had altered growth trajectories. In neonates, only the relative lung weight was reduced. In addition, an increased protein:DNA ratio indicated hypertrophy in fetal kidneys. Vitamin A injection had no additional effect on length of gestation and fetal or neonatal number. However, injection increased relative fetal organ weights in the VAF group but did not alter the effects of vitamin A deficiency in the neonate. These data suggest that chronic vitamin A deficiency during pregnancy compromises liver, heart and kidney and impairs lung growth and development during the last few days of gestation and reduces number of live neonates at birth.

Animals↗
PubMed1999

Effects of pre- and post-mating nutritional status on hepatic function, progesterone concentration, uterine protein secretion and embryo survival in Meishan pigs.

This experiment examined whether the pre- or the post-mating diet had greater impact on embryo survival in Meishan gilts. Gilts received either a maintenance (1.15 kg day(-1); n = 12) or a high (3.5 kg day(-1); n = 12) diet during the oestrous cycle preceding mating. After mating, half the animals in each group received either the maintenance or the high diet until slaughter on Day 12. Gilts fed the high pre-mating diet had more corpora lutea (22.7 v. 19.0, SED = 0.98; P<0.001), increased embryo survival (95.5% v. 74.8%, SED = 7.58; P<0.01) and heavier corpora lutea (-0.71 log g v. -0.90 log g, SED = 0.09; P = 0.07) compared with gilts fed the maintenance diet prior to mating. The post-mating diet had no effect on embryo survival. There were no treatment effects on blastocyst developmental stage, luteal surface area or progesterone release. Gilts receiving the high post-mating diet had heavier livers than those fed the maintenance post-mating diet (1.45 v 1.08% of total bodyweight, SED = 0.07; P<0.001), suggesting that these gilts have a greater capacity to metabolize progesterone. Pre-mating nutritional status therefore appears to be a greater determinant of embryo numbers and survival than the post-mating diet.

Acid Phosphatase↗
PubMed1999

Effects of pre- and post-mating feed intake on blastocyst size, secretory function and glucose metabolism in meishan gilts.

This experiment was designed to determine the effects of a nutritional regime, known to increase embryo survival, on blastocyst development and function. Day 12 blastocysts were recovered from Meishan gilts allocated in a 2x2 factorial design to receive either a high or a maintenance diet before or after mating (n = 4-6 gilts per group). The post-mating diet had no effect on individual blastocyst size, cell number, secretion of oestradiol-17beta or retinol binding protein, glucose metabolism or on the within-litter variability in these measures. Blastocysts recovered from gilts consuming the high pre-mating diet had more cells (13.501 v. 13.006 log cells; SED = 0.23; P = 0.05), greater production of CO2 from glucose (2.19 v. 1.23 log pmol(-1) blastocyst(-1) 3 h(-1), SED = 0.42; P = 0.05) and a lower within-litter standard deviation in blastocyst surface area (0.66 v. 1.18 log mm2, SED = 0.24; P = 0.04) compared with gilts fed the maintenance pre-mating diet. Collectively, these data suggest that a nutritional strategy that increases embryo survival is also associated with an increase in individual blastocyst cell number and reduced within-litter variability in blastocyst size.

Animal Nutritional Physiological Phenomena↗
PubMed1999

Expression of the growth arrest genes (GAS and GADD) changes during organogenesis in the rat fetus.

Mammalian cells mount an active response to nutrient limitation by overexpressing the growth arrest specific (GAS) and the growth arrest and DNA damage (GADD) genes. During embryogenesis in rats, there are quantitative and temporal differences in GAS and GADD gene expression during the development of the placenta, heart and kidney. Genes associated with the inhibition of DNA synthesis (p53 and GAS1) were predominantly expressed during the early stages of development, whereas those genes associated with inhibition of protein synthesis [GADD153 (also known as CHOP-10 or Ddit3) and C/EBP-beta] were more highly expressed during the later stages. The GADD45 gene was expressed throughout development. There were distinct periods of GAS3 and GAS6 gene expression during the development of the placenta, heart and kidneys, which is consistent with the proposed roles of these genes in cell interactions. These results show that there is a change in the expression of genes associated with the negative regulation of growth as the fetus develops.

Analysis of Variance↗
PubMed1999

The effects of maternal protein restriction on the growth of the rat fetus and its amino acid supply.

Maternal protein deficiency causes fetal growth retardation which has been associated with the programming of adult disease. The growth of the rat fetus was examined when the mothers were fed on diets containing 180, 90 and 60 g protein/kg. The numbers of fetuses were similar in animals fed on the 180 and 90 g protein/kg diets but the number was significantly reduced in the animals fed on the 60 g protein/kg diet. The fetuses carried by the mothers fed on the 90 g protein/kg diet were 7.5% heavier than those of mothers fed on 180 g protein/kg diet on day 19 of gestation, but by day 21 the situation was reversed and the fetuses in the protein-deficient mothers were 14% smaller. Analysis of the free amino acids in the maternal serum showed that on day 19 the diets containing 90 and 60 g protein/kg led to threonine concentrations that were reduced to 46 and 20% of those found in animals fed on the control (180 g/kg) diet. The other essential amino acids were unchanged, except for a small decrease in the branched-chain amino acids in animals fed on the 60 g protein/kg diet. Both low-protein diets significantly increased the concentrations of glutamic acid+glutamine and glycine in the maternal serum. On day 21 the maternal serum threonine levels were still reduced by about one third in the group fed on the 90 g protein/kg diet. Dietary protein content had no effect on serum threonine concentrations in nonpregnant animals. Analysis of the total free amino acids in the fetuses on day 19 showed that feeding the mother on a low-protein diet did not change amino acid concentrations apart from a decrease in threonine concentrations to 45 and 26% of the control values at 90 and 60 g protein/ kg respectively. The results suggest that threonine is of particular importance to the protein-deficient mother and her fetuses. Possible mechanisms for the decrease in free threonine in both mother and fetuses and the consequences of the change in amino acid metabolism are discussed.

Amino Acids↗
PubMed1999

Cytokines and the regulation of apoptosis in reproductive tissues: a review.

PROBLEM: To determine the role of apoptosis-regulating genes bax and bcl-2 in reproduction. METHOD OF STUDY: Review of literature and current data. RESULTS: The bcl-2 family of apoptotic regulatory gene products interact and form dimers of anti- and pro-apoptotic proteins (e.g., bcl-2 and bax respectively), the ratio of which determines cell death or survival. Menses is associated with increased apoptosis in the glands, a change in bcl-2:bax ratio and increased levels of the pro-apoptotic cytokine TNFalpha. Apoptosis occurs in all placental cell types and increases from first to third trimester. Placental apoptosis is induced by TNFalpha in vitro and increased levels in utero characterize most failing pregnancies, intra-uterine growth restriction (IUGR) and labour. An increased bcl-2:bax ratio and apoptosis in the syncytiotrophoblast characterizes failing first trimester pregnancies. Apoptosis in the syncytiotrophoblast is also associated with IUGR. In a rat model, maternal vitamin A deficiency perturbs fetal development. This is associated with a placental infiltrate of TNFalpha positive neutrophils (day 20) and increased placental apoptosis in areas of infiltration. A similar infiltrate occurs in a mouse model of early pregnancy loss. In the fetal membranes, clusters of bcl-2 negative chorion trophoblast cells undergo apoptosis. This may allow passage of myometrial stimulatory factors that induce labour. CONCLUSION: The ratio of bcl-2:bax is crucial in the regulation of apoptosis, particularly in the human placenta. Changes in trophoblast apoptosis characterize (1) early pregnancy failure, (2) IUGR and (3) pre-term and term labour. Regardless of gestational age, TNFalpha plays a major role in the induction of placental apoptosis.

Animals↗
PubMed1998

Effects of maternal vitamin A status on fetal heart and lung: changes in expression of key developmental genes.

Vitamin A is required during pregnancy for fetal lung development. These experiments monitored fetal lung morphology in normal and vitamin A-deficient rats. The expression of elastin and the growth arrest-specific gene 6 (gas6) in fetal and neonatal hearts and lungs was assessed by Northern blotting. In normal-fed rats, elastin and gas6 were expressed in the fetal lung and heart from day 19 of gestation up to day 2 postnatally. Maternal vitamin A deficiency altered fetal lung development. On day 20, the bronchial passageways were less developed and showed reduced staining for elastic fibers, and in the neonates, the relative air space and the size of the sacculi were reduced. In the fetal lung, the mRNAs for elastin and gas6 were reduced to 56 and 68% of the control values, respectively. In the fetal heart, the mRNA for elastin was reduced to 64% of the control value, whereas gas6 was increased twofold. In the neonate, there was no change in elastin expression in the lung or heart, but gas6 expression in the heart was increased twofold. These results suggest that, in the pregnant rat, vitamin A deficiency may retard fetal lung development or influence the differentiation of critical cell lines. The changes in elastin and gas6 expression may be used to identify the cell types affected.

Animals↗