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Maternal Supplementation (maternal + supplementation)
Selected AbstractsTetrahydrobiopterin in the prevention of hypertonia in hypoxic fetal brain,ANNALS OF NEUROLOGY, Issue 3 2009Jeannette Vásquez-Vivar PhD Objective Tetrahydrobiopterin (BH4) deficiency is a cause of dystonia at birth. We hypothesized that BH4 is a developmental factor determining vulnerability of the immature fetal brain to hypoxic-ischemic injury and subsequent motor deficits in newborns. Methods Pregnant rabbits were subjected to 40-minute uterine ischemia, and fetal brains were investigated for global and focal changes in BH4. Newborn kits were assessed by neurobehavioral tests following vehicle and sepiapterin (BH4 analog) treatment of dams. Results Naive fetal brains at 70% gestation (E22) were severely deficient for BH4 compared with maternal and other fetal tissues. BH4 concentration rapidly increased normally in the perinatal period, with the highest concentrations found in the thalamus compared with basal ganglia, frontal, occipital, hippocampus, and parietal cortex. Global sustained 40-minute hypoxia-ischemia depleted BH4 in E22 thalamus and to a lesser extent in basal ganglia, but not in the frontal, occipital, and parietal regions. Maternal supplementation prior to hypoxia-ischemia with sepiapterin increased BH4 in all brain regions and especially in the thalamus, but did not increase the intermediary metabolite, 7,8-BH2. Sepiapterin treatment also reduced incidence of severe motor deficits and perinatal death following E22 hypoxia-ischemia. Interpretation We conclude that early developmental BH4 deficiency plays a critical role in hypoxic-ischemic brain injury. Increasing brain BH4 via maternal supplementation may be an effective strategy in preventing motor deficits from antenatal hypoxia-ischemia. Ann Neurol 2009;66:323,331 [source] The genetic background of the curly tail strain confers susceptibility to folate-deficiency-induced exencephalyBIRTH DEFECTS RESEARCH, Issue 2 2010Katie A. Burren Abstract BACKGROUND: Suboptimal maternal folate status is considered a risk factor for neural tube defects (NTDs). However, the relationship between dietary folate status and risk of NTDs appears complex, as experimentally induced folate deficiency is insufficient to cause NTDs in nonmutant mice. In contrast, folate deficiency can exacerbate the effect of an NTD-causing mutation, as in splotch mice. The purpose of the present study was to determine whether folate deficiency can induce NTDs in mice with a permissive genetic background which do not normally exhibit defects. METHODS: Folate deficiency was induced in curly tail and genetically matched wild-type mice, and we analyzed the effect on maternal folate status, embryonic growth and development, and frequency of NTDs. RESULTS: Folate-deficient diets resulted in reduced maternal blood folate, elevated homocysteine, and a diminished embryonic folate content. Folate deficiency had a deleterious effect on reproductive success, resulting in smaller litter sizes and an increased rate of resorption. Notably, folate deficiency caused a similar-sized, statistically significant increase in the frequency of cranial NTDs among both curly tail (Grhl3 mutant) embryos and background-matched embryos that are wild type for Grhl3. The latter do not exhibit NTDs under normal dietary conditions. Maternal supplementation with myo -inositol reduced the incidence of NTDs in the folate-deficient wild-type strain. CONCLUSIONS: Dietary folate deficiency can induce cranial NTDs in nonmutant mice with a permissive genetic background, a situation that likely parallels gene-nutrient interactions in human NTDs. Our findings suggest that inositol supplementation may ameliorate NTDs resulting from insufficient dietary folate. Birth Defects Research (Part A), 2010. © 2009 Wiley-Liss, Inc. [source] Cardiovascular abnormalities in Folr1 knockout mice and folate rescue,BIRTH DEFECTS RESEARCH, Issue 4 2007Huiping Zhu Abstract BACKGROUND: Periconceptional folic acid supplementation is widely believed to aid in the prevention of neural tube defects (NTDs), orofacial clefts, and congenital heart defects. Folate-binding proteins or receptors serve to bind folic acid and 5-methyltetrahydrofolate, representing one of the two major mechanisms of cellular folate uptake. METHODS: We herein describe abnormal cardiovascular development in mouse fetuses lacking a functional folate-binding protein gene (Folr1). We also performed a dose-response study with folinic acid and determined the impact of maternal folate supplementation on Folr1 nullizygous cardiac development. RESULTS: Partially rescued preterm Folr1,/, (formerly referred to as Folbp1) fetuses were found to have outflow tract defects, aortic arch artery abnormalities, and isolated dextracardia. Maternal supplementation with folinic acid rescued the embryonic lethality and the observed cardiovascular phenotypes in a dose-dependant manner. Maternal genotype exhibited significant impact on the rescue efficiency, suggesting an important role of in utero folate status in embryonic development. Abnormal heart looping was observed during early development of Folr1,/, embryos partially rescued by maternal folinic acid supplementation. Migration pattern of cardiac neural crest cells, genetic signals in pharyngeal arches, and the secondary heart field were also found to be affected in the mutant embryos. CONCLUSIONS: Our observations suggest that the beneficial effect of folic acid for congenital heart defects might be mediated via its impact on neural crest cells and by gene regulation of signaling pathways involved in the development of the pharyngeal arches and the secondary heart field. Birth Defects Research (Part A) 2007. © 2007 Wiley-Liss, Inc. [source] Sex-related effects of maternal egg investment on offspring in relation to carotenoid availability in the great titJOURNAL OF ANIMAL ECOLOGY, Issue 1 2008Anne Berthouly Summary 1Maternal carotenoids in the egg yolk have been hypothesized to promote maturation of the immune system and protect against free radical damages. Depending on availability, mothers may thus influence offspring quality by depositing variable amounts of carotenoids into the eggs. Sex allocation theory predicts that in good quality environments, females should invest into offspring of the sex that will provide larger fitness return, generally males. 2In a field experiment we tested whether female great tits bias their investment towards males when carotenoid availability is increased, and whether male offspring of carotenoid-supplemented mothers show higher body condition. We partially cross-fostered hatchlings to disentangle maternal effects from post-hatching effects, and manipulated hen flea Ceratophyllus gallinae infestation to investigate the relationship between carotenoid availability and resistance to ectoparasites. 3As predicted, we found that carotenoid-supplemented mothers produced males that were heavier than their sisters at hatching, while the reverse was true for control mothers. This suggests that carotenoid availability during egg production affects male and female hatchlings differentially, possibly via a differential allocation to male and female eggs. 4A main effect of maternal supplementation became visible 14 days after hatching when nestlings hatched from eggs laid by carotenoid-supplemented mothers had gained significantly more mass than control nestlings. Independently of the carotenoid treatment, fleas impaired mass gain of nestlings during the first 9 days in large broods only and reduced tarsus length of male nestlings at an age of 14 days, suggesting a cost to mount a defence against parasites. 5Overall, our results suggest that pre-laying availability of carotenoids affects nestling condition in a sex-specific way with potentially longer-lasting effects on offspring fitness. [source] In Vivo Dysfunction of the Term Alveolar Macrophage After in Utero Ethanol ExposureALCOHOLISM, Issue 2 2007Xiao-Du Ping Background: The effects of in utero alcohol exposure on the immune function of the newborn remain under investigation. Fetal ethanol (ETOH) exposure increases oxidative stress in the developing lung, in part due to decreased availability of the antioxidant glutathione (GSH). We have previously shown that in utero ETOH impairs alveolar macrophage phagocytosis and viability in the premature pup, while maintaining GSH availability with maternal supplementation of S -adenosyl-methionine (SAM) during ETOH ingestion improves macrophage function and viability. We hypothesized that dysfunction of the neonatal alveolar macrophage exposed to ETOH in utero would persist at term gestation. Methods: Using a guinea-pig model of fetal ETOH exposure, timed-pregnant guinea-pigs were pair-fed ETOH±the GSH precursor SAM and the diet continued until spontaneous delivery. Term alveolar macrophages were evaluated using fluorescent microscopy for phagocytosis and apoptosis after in vitro incubation with Staphalococcus aureus. Using an in vivo model of intranasal Staph. aureus inoculation, the in vivo function of the term alveolar macrophage was also investigated using confocal fluorescent analysis. Results: In utero ETOH exposure increased oxidant stress in the alveolar macrophage and decreased phagocytosis and viability in vitro and in vivo. Confocal analysis of phagocytosis in vivo demonstrated a marked impairment of internalization of the bacteria by the ETOH-exposed alveolar macrophage. The addition of SAM during maternal ETOH ingestion prevented loss of alveolar macrophage function and viability in vitro and in vivo. Conclusions: In utero ETOH exposure impairs alveolar macrophage function and viability in vitro and in vivo even at term gestation. The ETOH-induced changes in macrophage function and viability can be ablated with maternal SAM supplementation. Further investigations are required to identify the mechanisms of ETOH-induced derangement of phagocytosis in the neonatal alveolar macrophage and the clinical ramifications of altered immune function after in utero alcohol exposure for the newborn. [source] Tetrahydrobiopterin in the prevention of hypertonia in hypoxic fetal brain,ANNALS OF NEUROLOGY, Issue 3 2009Jeannette Vásquez-Vivar PhD Objective Tetrahydrobiopterin (BH4) deficiency is a cause of dystonia at birth. We hypothesized that BH4 is a developmental factor determining vulnerability of the immature fetal brain to hypoxic-ischemic injury and subsequent motor deficits in newborns. Methods Pregnant rabbits were subjected to 40-minute uterine ischemia, and fetal brains were investigated for global and focal changes in BH4. Newborn kits were assessed by neurobehavioral tests following vehicle and sepiapterin (BH4 analog) treatment of dams. Results Naive fetal brains at 70% gestation (E22) were severely deficient for BH4 compared with maternal and other fetal tissues. BH4 concentration rapidly increased normally in the perinatal period, with the highest concentrations found in the thalamus compared with basal ganglia, frontal, occipital, hippocampus, and parietal cortex. Global sustained 40-minute hypoxia-ischemia depleted BH4 in E22 thalamus and to a lesser extent in basal ganglia, but not in the frontal, occipital, and parietal regions. Maternal supplementation prior to hypoxia-ischemia with sepiapterin increased BH4 in all brain regions and especially in the thalamus, but did not increase the intermediary metabolite, 7,8-BH2. Sepiapterin treatment also reduced incidence of severe motor deficits and perinatal death following E22 hypoxia-ischemia. Interpretation We conclude that early developmental BH4 deficiency plays a critical role in hypoxic-ischemic brain injury. Increasing brain BH4 via maternal supplementation may be an effective strategy in preventing motor deficits from antenatal hypoxia-ischemia. Ann Neurol 2009;66:323,331 [source] Fish oil supplementation in pregnancy and lactation may decrease the risk of infant allergyACTA PAEDIATRICA, Issue 9 2009Catrin Furuhjelm Abstract Maternal intake of omega- 3 (,-3) polyunsaturated fatty acids (PUFAs) during pregnancy has decreased, possibly contributing to a current increased risk of childhood allergy. Aim:, To describe the effects of maternal ,-3 long-chain PUFA supplementation during pregnancy and lactation on the incidence of allergic disease in infancy. Methods:, One hundred and forty-five pregnant women, affected by allergy themselves or having a husband or previous child with allergies, were included in a randomized placebo-controlled trial. Daily maternal supplementation with either 1.6 g eicosapentaenoic acid and 1.1 g docosahexaenoic acid or placebo was given from the 25th gestational week to average 3,4 months of breastfeeding. Skin prick tests, detection of circulating specific immunoglobulin E (IgE) antibodies and clinical examinations of the infants were performed. Results:, The period prevalence of food allergy was lower in the ,-3 group (1/52, 2%) compared to the placebo group (10/65, 15%, p < 0.05) as well as the incidence of IgE-associated eczema (,-3 group: 4/52, 8%; placebo group: 15/63, 24%, p < 0.05). Conclusion:, Maternal ,-3 fatty acid supplementation may decrease the risk of food allergy and IgE-associated eczema during the first year of life in infants with a family history of allergic disease. [source] Early-life nutritional and environmental determinants of thymic size in infants born in rural BangladeshACTA PAEDIATRICA, Issue 7 2009SE Moore Abstract Aim:, The aim was to assess the impact of nutritional status and environmental exposures on infant thymic development in the rural Matlab region of Bangladesh. Methods:, In a cohort of Nmax 2094 infants born during a randomized study of combined interventions to improve maternal and infant health, thymic volume (thymic index, TI) was assessed by ultrasonography at birth and at 8, 24 and 52 weeks of age. Data on birth weight, infant anthropometry and feeding status were also collected. Results:, At all ages, TI was positively associated with infant weight and strongly associated with the month of measurement. Longer duration of exclusive breastfeeding resulted in a larger TI at 52 weeks. TI at birth and at 8 weeks correlated positively with birth weight, but by 24 and 52 weeks and when adjusted for infant weight this effect was no longer present. Thymic size was not affected by pre-natal maternal supplementation or by socioeconomic status but was correlated to arsenic exposure during pregnancy. Conclusion:, In this population of rural Bangladeshi infants, thymic development is influenced by both nutritional and environmental exposures early in life. The long-term functional implications of these findings warrant further investigation. [source] | |||||||||||||