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Microarray Analysis Reveals Higher Gestational Folic Acid Alters Expression of Genes in the Cerebellum of Mice Offspring—A Pilot Study  [PDF]
Subit Barua,Salomon Kuizon,Kathryn K. Chadman,W. Ted Brown,Mohammed A. Junaid
Brain Sciences , 2015, DOI: 10.3390/brainsci5010014
Abstract: Folate is a water-soluble vitamin that is critical for nucleotide synthesis and can modulate methylation of DNA by altering one-carbon metabolism. Previous studies have shown that folate status during pregnancy is associated with various congenital defects including the risk of aberrant neural tube closure. Maternal exposure to a methyl supplemented diet also can alter DNA methylation and gene expression, which may influence the phenotype of offspring. We investigated if higher gestational folic acid (FA) in the diet dysregulates the expression of genes in the cerebellum of offspring in C57BL/6 J mice. One week before gestation and throughout the pregnancy, groups of dams were supplemented with FA either at 2 mg/kg or 20 mg/kg of diet. Microarray analysis was used to investigate the genome wide gene expression profile in the cerebellum from day old pups. Our results revealed that exposure to the higher dose FA diet during gestation dysregulated expression of several genes in the cerebellum of both male and female pups. Several transcription factors, imprinted genes, neuro-developmental genes and genes associated with autism spectrum disorder exhibited altered expression levels. These findings suggest that higher gestational FA potentially dysregulates gene expression in the offspring brain and such changes may adversely alter fetal programming and overall brain development.
No Effect of Folic Acid Supplementation on Global DNA Methylation in Men and Women with Moderately Elevated Homocysteine  [PDF]
Audrey Y. Jung, Yvo Smulders, Petra Verhoef, Frans J. Kok, Henk Blom, Robert M. Kok, Ellen Kampman, Jane Durga
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0024976
Abstract: A global loss of cytosine methylation in DNA has been implicated in a wide range of diseases. There is growing evidence that modifications in DNA methylation can be brought about by altering the intake of methyl donors such as folate. We examined whether long-term daily supplementation with 0.8 mg of folic acid would increase global DNA methylation compared with placebo in individuals with elevated plasma homocysteine. We also investigated if these effects were modified by MTHFR C677T genotype. Two hundred sixteen participants out of 818 subjects who had participated in a randomized double-blind placebo-controlled trial were selected, pre-stratified on MTHFR C677T genotype and matched on age and smoking status. They were allocated to receive either folic acid (0.8 mg/d; n = 105) or placebo treatment (n = 111) for three years. Peripheral blood leukocyte DNA methylation and serum and erythrocyte folate were assessed. Global DNA methylation was measured using liquid chromatography-tandem mass spectrometry and expressed as a percentage of 5-methylcytosines versus the total number of cytosine. There was no difference in global DNA methylation between those randomized to folic acid and those in the placebo group (difference = 0.008, 95%CI = ?0.05,0.07, P = 0.79). There was also no difference between treatment groups when we stratified for MTHFR C677T genotype (CC, n = 76; CT, n = 70; TT, n = 70), baseline erythrocyte folate status or baseline DNA methylation levels. In moderately hyperhomocysteinemic men and women, long-term folic acid supplementation does not increase global DNA methylation in peripheral blood leukocytes. ClinicalTrials.gov NCT00110604
High Folic Acid Intake during Pregnancy Lowers Body Weight and Reduces Femoral Area and Strength in Female Rat Offspring  [PDF]
Pedro S. P. Huot,David W. Dodington,Rebecca C. Mollard,Sandra A. Reza-López,Diana Sánchez-Hernández,Clara E. Cho,Justin Kuk,Wendy E. Ward,G. Harvey Anderson
Journal of Osteoporosis , 2013, DOI: 10.1155/2013/154109
Abstract: Rats fed gestational diets high in multivitamin or folate produce offspring of altered phenotypes. We hypothesized that female rat offspring born to dams fed a gestational diet high in folic acid (HFol) have compromised bone health and that feeding the offspring the same HFol diet attenuates these effects. Pregnant rats were fed diets with either recommended folic acid (RFol) or 10-fold higher folic acid (HFol) amounts. Female offspring were weaned to either the RFol or HFol diet for 17 weeks. HFol maternal diet resulted in lower offspring body weights (6%, ) and, after adjusting for body weight and femoral length, smaller femoral area (2%, ), compared to control diet. After adjustments, HFol pup diet resulted in lower mineral content (7%, ) and density (4%, ) of lumbar vertebra 4 without differences in strength. An interaction between folate content of the dam and pup diets revealed that a mismatch resulted in lower femoral peak load strength ( ) and stiffness ( ). However, the match in folate content failed to prevent lower weight gain. In conclusion, HFol diets fed to rat dams and their offspring affect area and strength of femurs and mineral quantity but not strength of lumbar vertebrae in the offspring. 1. Introduction Osteoporosis is a major public health concern in North America and affects as many as 2 million Canadians [1] and 40 million Americans [2]. The financial burden of long-term, hospital, and chronic care of osteoporosis is estimated to be $2.3 billion dollars per year in Canada [3] and greater than $15 billion dollars per year in the United States [4]. Adult bone health and risk of osteoporosis is dictated, in part, by whether individuals achieve peak bone mass by young adulthood [2, 5]. Peak bone mass is controlled by genetics as well as lifestyle factors including diet and physical activity. Epidemiological evidence suggests that many children from families with history of fractures have lower bone mass, and therefore higher risk for fractures [2]. Moreover, appropriate nutrition during pregnancy and in early childhood is essential in maintaining bone health and can alter the trajectory of achieving peak bone mass (as reviewed in [5–7]). The interest in folic acid intake during pregnancy and childhood and its effects on bone health is twofold. First, higher intake of folic acid is associated with higher bone mineral density (BMD) of postmenopausal women older than 50 [8, 9] and is associated with a lower risk of fractures in men and women older than 65 [10, 11]. Second, early diet may modulate the risk of developing diseases in
Maternal High Fat Feeding Does Not Have Long-Lasting Effects on Body Composition and Bone Health in Female and Male Wistar Rat Offspring at Young Adulthood  [PDF]
Paula M. Miotto,Laura M. Castelli,Foyinsola Amoye,Paul J. LeBlanc,Sandra J. Peters,Brian D. Roy,Wendy E. Ward
Molecules , 2013, DOI: 10.3390/molecules181215094
Abstract: High fat diets adversely affect body composition, bone mineral and strength, and alter bone fatty acid composition. It is unclear if maternal high fat (HF) feeding permanently alters offspring body composition and bone health. Female rats were fed control (CON) or HF diet for 10 weeks, bred, and continued their diets throughout pregnancy and lactation. Male and female offspring were studied at weaning and 3 months, following consumption of CON diet. At weaning, but not 3 months of age, male and female offspring from dams fed HF diet had lower lean mass and higher fat and bone mass, and higher femur bone mineral density (females only) than offspring of dams fed CON diet. Male and female offspring femurs from dams fed HF diet had higher monounsaturates and lower n6 polyunsaturates at weaning than offspring from dams fed CON diet, where females from dams fed HF diet had higher saturates and lower n6 polyunsaturates at 3 months of age. There were no differences in strength of femurs or lumbar vertebrae at 3 months of age in either male or female offspring. In conclusion, maternal HF feeding did not permanently affect body composition and bone health at young adulthood in offspring.
Maternal Ethanol Consumption Alters the Epigenotype and the Phenotype of Offspring in a Mouse Model  [PDF]
Nina Kaminen-Ahola,Arttu Ahola,Murat Maga,Kylie-Ann Mallitt,Paul Fahey,Timothy C. Cox,Emma Whitelaw,Suyinn Chong
PLOS Genetics , 2010, DOI: 10.1371/journal.pgen.1000811
Abstract: Recent studies have shown that exposure to some nutritional supplements and chemicals in utero can affect the epigenome of the developing mouse embryo, resulting in adult disease. Our hypothesis is that epigenetics is also involved in the gestational programming of adult phenotype by alcohol. We have developed a model of gestational ethanol exposure in the mouse based on maternal ad libitum ingestion of 10% (v/v) ethanol between gestational days 0.5–8.5 and observed changes in the expression of an epigenetically-sensitive allele, Agouti viable yellow (Avy), in the offspring. We found that exposure to ethanol increases the probability of transcriptional silencing at this locus, resulting in more mice with an agouti-colored coat. As expected, transcriptional silencing correlated with hypermethylation at Avy. This demonstrates, for the first time, that ethanol can affect adult phenotype by altering the epigenotype of the early embryo. Interestingly, we also detected postnatal growth restriction and craniofacial dysmorphology reminiscent of fetal alcohol syndrome, in congenic a/a siblings of the Avy mice. These findings suggest that moderate ethanol exposure in utero is capable of inducing changes in the expression of genes other than Avy, a conclusion supported by our genome-wide analysis of gene expression in these mice. In addition, offspring of female mice given free access to 10% (v/v) ethanol for four days per week for ten weeks prior to conception also showed increased transcriptional silencing of the Avy allele. Our work raises the possibility of a role for epigenetics in the etiology of fetal alcohol spectrum disorders, and it provides a mouse model that will be a useful resource in the continued efforts to understand the consequences of gestational alcohol exposure at the molecular level.
The Effect of Neonatal Leptin Antagonism in Male Rat Offspring Is Dependent upon the Interaction between Prior Maternal Nutritional Status and Post-Weaning Diet  [PDF]
J. Beltrand,D. M. Sloboda,K. L. Connor,M. Truong,M. H. Vickers
Journal of Nutrition and Metabolism , 2012, DOI: 10.1155/2012/296935
Abstract: Epidemiological and experimental studies report associations between overweight mothers and increased obesity risk in offspring. It is unclear whether neonatal leptin regulation mediates this association between overweight mothers and offspring obesity. We investigated the effect of neonatal treatment with a leptin antagonist (LA) on growth and metabolism in offspring of mothers fed either a control or a high fat diet. Wistar rats were fed either a control (CON) or a high fat diet (MHF) during pregnancy and lactation. Male CON and MHF neonates received either saline (S) or a rat-specific pegylated LA on days 3, 5, and 7. Offspring were weaned onto either a control or a high fat (hf) diet. At day 100, body composition, blood glucose, β-hydroxybutyrate and plasma leptin and insulin were determined. In CON and MHF offspring, LA increased neonatal bodyweights compared to saline-treated offspring and was more pronounced in MHF offspring. In the post-weaning period, neonatal LA treatment decreased hf diet-induced weight gain but only in CON offspring. LA treatment induced changes in body length, fat mass, body temperature, and bone composition. Neonatal LA treatment can therefore exert effects on growth and metabolism in adulthood but is dependent upon interactions between maternal and post-weaning nutrition.
Pre-Weaning Growth Hormone Treatment Reverses Hypertension and Endothelial Dysfunction in Adult Male Offspring of Mothers Undernourished during Pregnancy  [PDF]
Clint Gray, Minglan Li, Clare M. Reynolds, Mark H. Vickers
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0053505
Abstract: Maternal undernutrition results in elevated blood pressure (BP) and endothelial dysfunction in adult offspring. However, few studies have investigated interventions during early life to ameliorate the programming of hypertension and vascular disorders. We have utilised a model of maternal undernutrition to examine the effects of pre-weaning growth hormone (GH) treatment on BP and vascular function in adulthood. Female Sprague-Dawley rats were fed either a standard control diet (CON) or 50% of CON intake throughout pregnancy (UN). From neonatal day 3 until weaning (day 21), CON and UN pups received either saline (CON-S, UN-S) or GH (2.5 ug/g/day)(CON-GH, UN-GH). All dams were fed ad libitum throughout lactation. Male offspring were fed a standard diet until the end of the study. Systolic blood pressure (SBP) was measured at day 150 by tail cuff plethysmography. At day 160, intact mesenteric vessels mounted on a pressure myograph. Responses to pressure, agonist-induced constriction and endothelium-dependent vasodilators were investigated to determine vascular function. SBP was increased in UN-S groups and normalised in UN-GH groups (CON-S 121±2 mmHg, CON-GH 115±3, UN-S 146±3, UN-GH 127±2). Pressure mediated dilation was reduced in UN-S offspring and normalised in UN-GH groups. Vessels from UN-S offspring demonstrated a reduced constrictor response to phenylephrine and reduced vasodilator response to acetylcholine (ACh). Furthermore, UN-S offspring vessels displayed a reduced vasodilator response in the presence of L-NG-Nitroarginine Methyl Ester (L-NAME), carbenoxolone (CBX), L-NAME and CBX, Tram-34 and Apamin. UN-GH vessels showed little difference in responses when compared to CON and significantly increased vasodilator responses when compared to UN-S offspring. Pre-weaning GH treatment reverses the negative effects of maternal UN on SBP and vasomotor function in adult offspring. These data suggest that developmental cardiovascular programming is potentially reversible by early life GH treatment and that GH can reverse the vascular adaptations resulting from maternal undernutrition.
The Effect of Neonatal Leptin Antagonism in Male Rat Offspring Is Dependent upon the Interaction between Prior Maternal Nutritional Status and Post-Weaning Diet  [PDF]
J. Beltrand,D. M. Sloboda,K. L. Connor,M. Truong,M. H. Vickers
Journal of Nutrition and Metabolism , 2012, DOI: 10.1155/2012/296935
Abstract: Epidemiological and experimental studies report associations between overweight mothers and increased obesity risk in offspring. It is unclear whether neonatal leptin regulation mediates this association between overweight mothers and offspring obesity. We investigated the effect of neonatal treatment with a leptin antagonist (LA) on growth and metabolism in offspring of mothers fed either a control or a high fat diet. Wistar rats were fed either a control (CON) or a high fat diet (MHF) during pregnancy and lactation. Male CON and MHF neonates received either saline (S) or a rat-specific pegylated LA on days 3, 5, and 7. Offspring were weaned onto either a control or a high fat (hf) diet. At day 100, body composition, blood glucose, β-hydroxybutyrate and plasma leptin and insulin were determined. In CON and MHF offspring, LA increased neonatal bodyweights compared to saline-treated offspring and was more pronounced in MHF offspring. In the post-weaning period, neonatal LA treatment decreased hf diet-induced weight gain but only in CON offspring. LA treatment induced changes in body length, fat mass, body temperature, and bone composition. Neonatal LA treatment can therefore exert effects on growth and metabolism in adulthood but is dependent upon interactions between maternal and post-weaning nutrition. 1. Introduction Obesity and metabolic-related disorders are considered major health issues worldwide. Over the last decade, the incidence of obesity and overweight has almost doubled in developed countries and the trend is mirrored in developing nations that are transitioning to first-world economies [1]. Obesity results from an interaction of many factors including genetic, physiologic, behavioural, and environmental influences. However, the rapid increases in the rates of obesity suggest that environmental and behavioural influences, rather than genetic causes, are fuelling the present epidemic. Increasing evidence from both clinical and animal studies has highlighted the link between altered maternal nutrition and the risk of offspring developing obesity and the metabolic syndrome [2–5]. Initial epidemiological studies suggested that fetal growth restriction is correlated with later disease, implying that fetal nutritional deprivation may be a strong stimulus for developmental programming. However, although maternal nutrient deprivation has been well characterized in this context, in many societies, maternal and postnatal nutrition can be excessive. As a result, excessive weight gain and/or obesity are common nutritional problems complicating
WEANING
IRAM MANZOOR
The Professional Medical Journal , 2009,
Abstract: Objective: To evaluate the awareness & practices regarding weaning in lactating mothers of infants. Design: A cross sectional descriptive study. Setting: At pediatrics OPD in Ghurki Trust Teaching hospital, Lahore. Period: From October to December 2007. Methodology: A non probability convenience sampling was done to collect data from 50 mothers who were attending out patient department along with their infants on a pre-formed questionnaire. After gathering, data was analyzed & presented in the form of tables & graphs. Results: In the present study, 66% mothers were in the age group of 20-29 years, all were house wives, 34 % were matriculate and 72% lived in joint family system, Mean age of weaning was 4-6 months in more than 64 % of the sample. Among the women interviewed, 44% used home-made weaning diets, 30% used mixture of homemade and commercially prepared diets, while 16% used only commercially prepared diets. Breast feeding was continued during and after weaning, by 64% of respondents along with weaning diets. Conclusion: Mothers need to be educated about the importance of weaning, the recommended age of weaning and about the types of weaning food. This can be achieved by using lady health workers and lady health visitors and the mass media. Importance of continued breast feeding with weaning diet should be emphasized upon.
An Interaction of the Pre- and Post-Weaning Diets Rich in Omega-6 Polyunsaturated Fats Alters Plasma Lipids, Hepatic Gene Expression and Aortic Vascular Reactivity in Adult C57Bl/6 Mice
Kanta Chechi, John J. Mcguire and Sukhinder K. Cheema
Nutrition and Metabolic Insights , 2012, DOI: 10.4137/NMI.S6026
Abstract: Aim: To investigate the effects of diets rich in n-6 polyunsaturated fats (PUFA) fed during pre- and post-weaning time periods on the lipid metabolism and vascular reactivity in adult C57Bl/6 mice, in order to assess the impact of maternal nutrition and its interaction with the offspring diet on the metabolism of adult offspring. Methods: Female C57Bl/6 mice were fed a high-fat diet enriched with n-6 PUFA (P) or control diet (C) for 2-weeks before, during mating, gestation and lactation, while their pups received either P or C for 8-weeks post-weaning. Results: A significant interaction between the maternal and post-weaning diets was observed for the offspring body weight, food-, caloric-intake, plasma lipids, hepatic mRNA expression of lecithin cholesterol acyltransferase, aortic contractile and relaxation responses (P < 0.05). Conclusion: The overall metabolic and physiological outcome in the offspring is dependent upon the interaction between the pre- and post-weaning dietary environments.
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