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Impaired Hypothalamic mTOR Activation in the Adult Rat Offspring Born to Mothers Fed a Low-Protein Diet  [PDF]
Omar Guzmán-Quevedo, Raquel Da Silva Arag?o, Georgina Pérez García, Rhowena J. B. Matos, André de Sa Braga Oliveira, Raul Manh?es de Castro, Francisco Bola?os-Jiménez
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0074990
Abstract: Several epidemiological and experimental studies have clearly established that maternal malnutrition induces a high risk of developing obesity and related metabolic diseases in the offspring. To determine if altered nutrient sensing might underlie this enhanced disease susceptibility, here we examined the effects of perinatal protein restriction on the activation of the nutrient sensor mTOR in response to acute variations in the nutritional status of the organism. Female Wistar rats were fed isocaloric diets containing either 17% protein (control) or 8% protein (PR) throughout pregnancy and lactation. At weaning offspring received standard chow and at 4 months of age the effects of fasting or fasting plus re-feeding on the phosphorylation levels of mTOR and its downstream target S6 ribosomal protein (rpS6) in the hypothalamus were assessed by immuno-fluorescence and western blot. Under ad libitum feeding conditions, PR rats exhibited decreased mTOR and rpS6 phosphorylation in the arcuate (ARC) and ventromedial (VMH) hypothalamic nuclei. Moreover, the phosphorylation of mTOR and rpS6 in these hypothalamic nuclei decreased with fasting in control but not in PR animals. Conversely, PR animals exhibited enhanced number of pmTOR imunostained cells in the paraventricular nucleus (PVN) and fasting decreased the activation of mTOR in the PVN of malnourished but not of control rats. These alterations occurred at a developmental stage at which perinatally-undernourished animals do not show yet obesity or glucose intolerance. Collectively, our observations suggest that altered hypothalamic nutrient sensing in response to an inadequate foetal and neonatal energetic environment is one of the basic mechanisms of the developmental programming of metabolic disorders and might play a causing role in the development of the metabolic syndrome induced by malnutrition during early life.
Maternal Melatonin Programs the Daily Pattern of Energy Metabolism in Adult Offspring  [PDF]
Danilo S. Ferreira, Fernanda G. Amaral, Caroline C. Mesquita, Ana Paula L. Barbosa, Camilo Lellis-Santos, Ariane O. Turati, Laila R. Santos, Carolina S. Sollon, Patricia R. Gomes, Juliana A. Faria, José Cipolla-Neto, Silvana Bordin, Gabriel F. Anhê
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0038795
Abstract: Background Shift work was recently described as a factor that increases the risk of Type 2 diabetes mellitus. In addition, rats born to mothers subjected to a phase shift throughout pregnancy are glucose intolerant. However, the mechanism by which a phase shift transmits metabolic information to the offspring has not been determined. Among several endocrine secretions, phase shifts in the light/dark cycle were described as altering the circadian profile of melatonin production by the pineal gland. The present study addresses the importance of maternal melatonin for the metabolic programming of the offspring. Methodology/Principal Findings Female Wistar rats were submitted to SHAM surgery or pinealectomy (PINX). The PINX rats were divided into two groups and received either melatonin (PM) or vehicle. The SHAM, the PINX vehicle and the PM females were housed with male Wistar rats. Rats were allowed to mate and after weaning, the male and female offspring were subjected to a glucose tolerance test (GTT), a pyruvate tolerance test (PTT) and an insulin tolerance test (ITT). Pancreatic islets were isolated for insulin secretion, and insulin signaling was assessed in the liver and in the skeletal muscle by western blots. We found that male and female rats born to PINX mothers display glucose intolerance at the end of the light phase of the light/dark cycle, but not at the beginning. We further demonstrate that impaired glucose-stimulated insulin secretion and hepatic insulin resistance are mechanisms that may contribute to glucose intolerance in the offspring of PINX mothers. The metabolic programming described here occurs due to an absence of maternal melatonin because the offspring born to PINX mothers treated with melatonin were not glucose intolerant. Conclusions/Significance The present results support the novel concept that maternal melatonin is responsible for the programming of the daily pattern of energy metabolism in their offspring.
Intuitive physics and intuitive psychology (“theory of mind”) in offspring of mothers with psychoses  [PDF]
Rebeka Marothi,Szabolcs Keri
PeerJ , 2015, DOI: 10.7287/peerj.preprints.248v1
Abstract: Offspring of individuals with psychoses sometimes display an abnormal development of cognition, language, motor performance, social adaptation, and emotional functions. The aim of this study was to investigate the ability of children of mothers with schizophrenia (n=28) and bipolar disorder (n=23) to understand mental states of others using the Eyes Test (folk psychology or “theory of mind”) and physical causal interactions of inanimate objects (folk psychics). Compared with healthy controls (n=29), the children of mothers with schizophrenia displayed significantly impaired performances on the Eyes Test but not on the folk physics test. The children of mothers with bipolar disorder did not differ from the controls and outperformed the children of mothers with schizophrenia on the folk physics test. These results suggest that the attribution of mental states, but not the interpretation of causal interaction of objects, is impaired in offspring of individuals with schizophrenia, which may contribute to social dysfunctions.
Methylation and Expression of Immune and Inflammatory Genes in the Offspring of Bariatric Bypass Surgery Patients  [PDF]
Frédéric Guénard,André Tchernof,Yves Deshaies,Katherine Cianflone,John G. Kral,Picard Marceau,Marie-Claude Vohl
Journal of Obesity , 2013, DOI: 10.1155/2013/492170
Abstract: Background. Maternal obesity, excess weight gain and overnutrition during pregnancy increase risks of obesity, type 2 diabetes mellitus, and cardiovascular disease in the offspring. Maternal biliopancreatic diversion is an effective treatment for severe obesity and is beneficial for offspring born after maternal surgery (AMS). These offspring exhibit lower severe obesity prevalence and improved cardiometabolic risk factors including inflammatory marker compared to siblings born before maternal surgery (BMS). Objective. To assess relationships between maternal bariatric surgery and the methylation/expression of genes involved in the immune and inflammatory pathways. Methods. A differential gene methylation analysis was conducted in a sibling cohort of 25 BMS and 25 AMS offspring from 20 mothers. Following differential gene expression analysis (23 BMS and 23 AMS), pathway analysis was conducted. Correlations between gene methylation/expression and circulating inflammatory markers were computed. Results. Five immune and inflammatory pathways with significant overrepresentation of both differential gene methylation and expression were identified. In the IL-8 pathway, gene methylation correlated with both gene expression and plasma C-reactive protein levels. Conclusion. These results suggest that improvements in cardiometabolic risk markers in AMS compared to BMS offspring may be mediated through differential methylation of genes involved in immune and inflammatory pathways. 1. Introduction Parental obesity increases the risk of obesity in offspring through genetic, biological, and environmental influences [1–3]. Maternal obesity, weight gain, and increased body mass index (BMI) between pregnancies and gestational diabetes increase risks of offspring obesity, type 2 diabetes mellitus (T2DM), and cardiovascular disease (CVD) in the offspring [4–7]. Consistent with the chronic low-grade inflammatory state of obesity, elevated concentrations of interleukin-6 (IL-6) and C-reactive protein (CRP) have been observed in obese pregnant women [8]. Higher maternal levels of IL-6 were predictive of the increased growth and adiposity in the offspring [9]. Maternal diet-induced obesity in sheep resulted in higher fetal triglyceride (TG) levels [10] and upregulated inflammatory signaling [11]. Offspring of rats injected with IL-6 throughout pregnancy had an altered inflammatory profile associated with greater body fat mass and reduced insulin sensitivity [12]. Epigenetic processes are important mediators of early-life environment, metabolism, and body composition in
Intuitive physics and intuitive psychology (“theory of mind”) in offspring of mothers with psychoses  [PDF]
Rebeka Maróthi,Szabolcs Kéri
PeerJ , 2015, DOI: 10.7717/peerj.330
Abstract: Offspring of individuals with psychoses sometimes display an abnormal development of cognition, language, motor performance, social adaptation, and emotional functions. The aim of this study was to investigate the ability of children of mothers with schizophrenia (n = 28) and bipolar disorder (n = 23) to understand mental states of others using the Eyes Test (folk psychology or “theory of mind”) and physical causal interactions of inanimate objects (folk physics). Compared with healthy controls (n = 29), the children of mothers with schizophrenia displayed significantly impaired performances on the Eyes Test but not on the folk physics test when corrected for IQ. The children of mothers with bipolar disorder did not differ from the controls. The folk physics test showed a significant covariance with IQ, whereas the Eyes Test did not exhibit such covariance. These results suggest that the attribution of mental states, but not the interpretation of causal interaction of objects, is impaired in offspring of individuals with schizophrenia, which may contribute to social dysfunctions.
Long-Lasting Effect of Perinatal Exposure to L-tryptophan on Circadian Clock of Primary Cell Lines Established from Male Offspring Born from Mothers Fed on Dietary Protein Restriction  [PDF]
Elizabeth Nascimento, Omar Guzman-Quevedo, Nellie Delacourt, Raquel da Silva Arag?o, Georgina Perez-Garcia, Sandra Lopes de Souza, Raul Manh?es-de-Castro, Francisco Bola?os-Jiménez, Bertrand Kaeffer
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0056231
Abstract: Background & Aims Maternal undernutrition programs metabolic adaptations which are ultimately detrimental to adult. L-tryptophan supplementation was given to manipulate the long-term sequelae of early-life programming by undernutrition and explore whether cultured cells retain circadian clock dysregulation. Methods Male rat pups from mothers fed on low protein (8%, LP) or control (18%, CP) diet were given, one hour before light off, an oral bolus of L-tryptophan (125 mg/kg) between Day-12 and Day-21 of age. Body weight, food intake, blood glucose along with the capacity of colonization of primary cells from biopsies were measured during the young (45–55 days) and adult (110–130 days) phases. Circadian clock oscillations were re-induced by a serum shock over 30 hours on near-confluent cell monolayers to follow PERIOD1 and CLOCK proteins by Fluorescent Linked ImmunoSorbent Assay (FLISA) and period1 and bmal1 mRNA by RT-PCR. Cell survival in amino acid-free conditions were used to measure circadian expression of MAP-LC3B, MAP-LC3B-FP and Survivin. Results Tryptophan supplementation did not alter body weight gain nor feeding pattern. By three-way ANOVA of blood glucose, sampling time was found significant during all phases. A significant interaction between daily bolus (Tryptophan, saline) and diets (LP, CP) were found during young (p = 0.0291) and adult (p = 0.0285) phases. In adult phase, the capacity of colonization at seeding of primary cells was twice lower for LP rats. By three-way ANOVA of PERIOD1 perinuclear/nuclear immunoreactivity during young phase, we found a significant effect of diets (p = 0.049), daily bolus (p<0.0001) and synchronizer hours (p = 0.0002). All factors were significantly interacting (p = 0.0148). MAP-LC3B, MAP-LC3B-FP and Survivin were altered according to diets in young phase. Conclusions Sequelae of early-life undernutrition and the effects of L-tryptophan supplementation can be monitored non-invasively by circadian sampling of blood D-glucose and on the expression of PERIOD1 protein in established primary cell lines.
Dynamic Reprogramming of DNA Methylation at an Epigenetically Sensitive Allele in Mice  [PDF]
Marnie E Blewitt,Nicola K Vickaryous,Andras Paldi,Haruhiko Koseki,Emma Whitelaw
PLOS Genetics , 2006, DOI: 10.1371/journal.pgen.0020049
Abstract: There is increasing evidence in both plants and animals that epigenetic marks are not always cleared between generations. Incomplete erasure at genes associated with a measurable phenotype results in unusual patterns of inheritance from one generation to the next, termed transgenerational epigenetic inheritance. The Agouti viable yellow (Avy) allele is the best-studied example of this phenomenon in mice. The Avy allele is the result of a retrotransposon insertion upstream of the Agouti gene. Expression at this locus is controlled by the long terminal repeat (LTR) of the retrotransposon, and expression results in a yellow coat and correlates with hypomethylation of the LTR. Isogenic mice display variable expressivity, resulting in mice with a range of coat colours, from yellow through to agouti. Agouti mice have a methylated LTR. The locus displays epigenetic inheritance following maternal but not paternal transmission; yellow mothers produce more yellow offspring than agouti mothers. We have analysed the DNA methylation in mature gametes, zygotes, and blastocysts and found that the paternally and maternally inherited alleles are treated differently. The paternally inherited allele is demethylated rapidly, and the maternal allele is demethylated more slowly, in a manner similar to that of nonimprinted single-copy genes. Interestingly, following maternal transmission of the allele, there is no DNA methylation in the blastocyst, suggesting that DNA methylation is not the inherited mark. We have independent support for this conclusion from studies that do not involve direct analysis of DNA methylation. Haplo-insufficiency for Mel18, a polycomb group protein, introduces epigenetic inheritance at a paternally derived Avy allele, and the pedigrees reveal that this occurs after zygotic genome activation and, therefore, despite the rapid demethylation of the locus.
Dynamic reprogramming of DNA methylation at an epigenetically sensitive allele in mice.  [cached]
Blewitt Marnie E,Vickaryous Nicola K,Paldi Andras,Koseki Haruhiko
PLOS Genetics , 2006,
Abstract: There is increasing evidence in both plants and animals that epigenetic marks are not always cleared between generations. Incomplete erasure at genes associated with a measurable phenotype results in unusual patterns of inheritance from one generation to the next, termed transgenerational epigenetic inheritance. The Agouti viable yellow (A(vy)) allele is the best-studied example of this phenomenon in mice. The A(vy) allele is the result of a retrotransposon insertion upstream of the Agouti gene. Expression at this locus is controlled by the long terminal repeat (LTR) of the retrotransposon, and expression results in a yellow coat and correlates with hypomethylation of the LTR. Isogenic mice display variable expressivity, resulting in mice with a range of coat colours, from yellow through to agouti. Agouti mice have a methylated LTR. The locus displays epigenetic inheritance following maternal but not paternal transmission; yellow mothers produce more yellow offspring than agouti mothers. We have analysed the DNA methylation in mature gametes, zygotes, and blastocysts and found that the paternally and maternally inherited alleles are treated differently. The paternally inherited allele is demethylated rapidly, and the maternal allele is demethylated more slowly, in a manner similar to that of nonimprinted single-copy genes. Interestingly, following maternal transmission of the allele, there is no DNA methylation in the blastocyst, suggesting that DNA methylation is not the inherited mark. We have independent support for this conclusion from studies that do not involve direct analysis of DNA methylation. Haplo-insufficiency for Mel18, a polycomb group protein, introduces epigenetic inheritance at a paternally derived A(vy) allele, and the pedigrees reveal that this occurs after zygotic genome activation and, therefore, despite the rapid demethylation of the locus.
Effects of Taurine Supplementation on Hepatic Markers of Inflammation and Lipid Metabolism in Mothers and Offspring in the Setting of Maternal Obesity  [PDF]
Minglan Li, Clare M. Reynolds, Deborah M. Sloboda, Clint Gray, Mark H. Vickers
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0076961
Abstract: Maternal obesity is associated with obesity and metabolic disorders in offspring. However, intervention strategies to reverse or ameliorate the effects of maternal obesity on offspring health are limited. Following maternal undernutrition, taurine supplementation can improve outcomes in offspring, possibly via effects on glucose homeostasis and insulin secretion. The effects of taurine in mediating inflammatory processes as a protective mechanism has not been investigated. Further, the efficacy of taurine supplementation in the setting of maternal obesity is not known. Using a model of maternal obesity, we examined the effects of maternal taurine supplementation on outcomes related to inflammation and lipid metabolism in mothers and neonates. Time-mated Wistar rats were randomised to either: 1) control : control diet during pregnancy and lactation (CON); 2) CON supplemented with 1.5% taurine in drinking water (CT); 3) maternal obesogenic diet (high fat, high fructose) during pregnancy and lactation (MO); or 4) MO supplemented with taurine (MOT). Maternal and neonatal weights, plasma cytokines and hepatic gene expression were analysed. A MO diet resulted in maternal hyperinsulinemia and hyperleptinemia and increased plasma glucose, glutamate and TNF-α concentrations. Taurine normalised maternal plasma TNF-α and glutamate concentrations in MOT animals. Both MO and MOT mothers displayed evidence of fatty liver accompanied by alterations in key markers of hepatic lipid metabolism. MO neonates displayed a pro-inflammatory hepatic profile which was partially rescued in MOT offspring. Conversely, a pro-inflammatory phenotype was observed in MOT mothers suggesting a possible maternal trade-off to protect the neonate. Despite protective effects of taurine in MOT offspring, neonatal mortality was increased in CT neonates, indicating possible adverse effects of taurine in the setting of normal pregnancy. These data suggest that maternal taurine supplementation may ameliorate the adverse effects observed in offspring following a maternal obesogenic diet but these effects are dependent upon prior maternal nutritional background.
PROLACTIN-Deficiency in Adult Offspring of Diabetic Mothers  [PDF]
Leona Aerts,Rieta Van Bree,F. André Van Assche
Experimental Diabetes Research , 2000, DOI: 10.1155/edr.2000.31
Abstract: Maternal diabetes induces fetal alterations, resulting in lasting consequences for the glucose tolerance of the offspring over several generations. In our experimental rat model, circulating prolactin, oestradiol, progesterone and corticosterone levels, known to influence insulin secretion and action, are determined in plasma of female adult offspring of mildly and severely diabetic mothers. Prolactin and progesterone levels are equally low in both groups as compared to controls, stressing the involvement of the CNS in the transgeneration effect; oestradiol and corticosterone levels are normal. No correlation is found between these hormonal alterations and the known differences in glucose tolerance.
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