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Alan D. Ealy - One of the best experts on this subject based on the ideXlab platform.
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Exposure to Maternal Obesity alters gene expression in the preimplantation ovine conceptus
BMC genomics, 2018Co-Authors: Sarah R. Mccoski, Mccauley T. Vailes, Connor E. Owens, Rebecca R Cockrum, Alan D. EalyAbstract:Background Embryonic and fetal exposure to Maternal Obesity causes several maladaptive morphological and epigenetic changes in exposed offspring. The timing of these events is unclear, but changes can be observed even after a short exposure to Maternal Obesity around the time of conception. The hypothesis of this work is that Maternal Obesity influences the ovine preimplantation conceptus early in pregnancy, and this exposure will affect gene expression in embryonic and extraembryonic tissues.
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Exposure to Maternal Obesity alters gene expression in the preimplantation ovine conceptus
BMC Genomics, 2018Co-Authors: Sarah R. Mccoski, Mccauley T. Vailes, Connor E. Owens, Rebecca R Cockrum, Alan D. EalyAbstract:Background Embryonic and fetal exposure to Maternal Obesity causes several maladaptive morphological and epigenetic changes in exposed offspring. The timing of these events is unclear, but changes can be observed even after a short exposure to Maternal Obesity around the time of conception. The hypothesis of this work is that Maternal Obesity influences the ovine preimplantation conceptus early in pregnancy, and this exposure will affect gene expression in embryonic and extraembryonic tissues. Results Obese and lean ewe groups were established by overfeeding or normal feeding, respectively. Ewes were then bred to genetically similar rams. Conceptuses were collected at day 14 of gestation. Morphological assessments were made, conceptuses were sexed by genomic PCR analysis, and samples underwent RNA-sequencing analysis. While no obvious morphological differences existed between conceptuses, differentially expressed genes (≥ 2-fold; ≥ 0.2 RPKM; ≤ 0.05 FDR) were detected based on Maternal Obesity exposure ( n = 21). Also, differential effects of Maternal Obesity were noted on each conceptus sex ( n = 347). A large portion of differentially expressed genes were associated with embryogenesis and placental development. Conclusions Findings reveal that the preimplantation ovine conceptus genome responds to Maternal Obesity in a sex-dependent manner. The sexual dimorphism in response to the Maternal environment coupled with changes in placental gene expression may explain aberrations in phenotype observed in offspring derived from obese females.
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Maternal Obesity alters the expression of embryonic regulatory transcripts in the preimplantation ovine conceptus.
Reproductive biology, 2018Co-Authors: Sarah R. Mccoski, Mccauley T. Vailes, Rebecca K. Poole, Alan D. EalyAbstract:Abstract The influence of exposure to overfeeding-induced Maternal Obesity around the time of conception on early embryogenesis was examined in the day 14 ovine conceptus. The relative abundance of FGFR2 and DNMT1 was influenced by Maternal Obesity status and conceptus sex, and the abundance of PPARG and PTGS2 transcripts was greater in male conceptuses regardless of the Obesity status of the ewe. These observations demonstrated that short-term exposure to Maternal Obesity impacts early conceptus transcript patterning.
Martha M Werler - One of the best experts on this subject based on the ideXlab platform.
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Maternal Obesity gestational diabetes and central nervous system birth defects
Obstetrical & Gynecological Survey, 2005Co-Authors: James L Anderson, Kim D Waller, Mark A Canfield, Gary M Shaw, Margaret L Watkins, Martha M WerlerAbstract:ABSTRACT Several large-scale cohort studies suggest that obese mothers are at increased risk of having infants with neural tube defects and, possibly, other central nervous system (CNS) birth defects. Because Obesity and diabetes share similar metabolic abnormalities, a study was planned to determine whether gestational diabetes influences the association between Maternal Obesity and CNS birth defects. In this population-based case–control study, covering the years 1997 to mid-2000, structured telephone interviews were conducted with mothers of offspring having anencephaly (n = 120), spina bifida (n = 184), holoprosencephaly (n = 49), or isolated hydrocephaly (n = 124). Control women whose infants were neurologically normal were randomly chosen from the same hospitals. Approximately 60% of both cases and control subjects responded. Maternal Obesity was defined as a body mass index of 30 kg/m2 or higher. Pregestational diabetes, both type 1 and type 2, correlated closely with holoprosencephaly (adjusted odds ratio [OR], 47; 95% confidence interval [CI], 9.5–230), and isolated hydrocephaly (OR, 12; 95% CI, 2.9–47). There was no increase in the risk of anencephaly or spina bifida. Gestational diabetes increased only the risk of holoprosencephaly (OR, 2.9; 95% CI, 1.0–8.4). Mothers of infants with anencephaly were less likely than control mothers to have gestational diabetes. Obese mothers were likelier than control subjects to have infants with any of the 4 CNS birth defects. Underweight women were less likely to have an infant with spina bifida. The association between Maternal Obesity and an increased risk of neural tube defects and isolated hydrocephaly held for all ethnic groups. Associations between Maternal Obesity and anencephaly (OR, 2.3; 95% CI, 1.2–4.3), spina bifida (OR, 2.8; 95% CI, 1.7–4.5), and isolated hydrocephaly (OR, 2.7; 95% CI, 1.5–5.0) persisted after adjusting for Maternal age, ethnicity, education, smoking, alcohol use, and periconceptional vitamin use. For both spina bifida and holoprosencephaly, the joint effects of Maternal Obesity and gestational diabetes appeared to be interactive. These findings suggest that gestational diabetes and Maternal Obesity may increase the risk of CNS birth defects through common mechanisms, and they strongly support the need for ways of preventing these conditions.
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Maternal Obesity gestational diabetes and central nervous system birth defects
Epidemiology, 2005Co-Authors: James L Anderson, Kim D Waller, Mark A Canfield, Gary M Shaw, Margaret L Watkins, Martha M WerlerAbstract:Background: Maternal Obesity and diabetes are both associated with increased risk of congenital central nervous system (CNS) malformations in the offspring and may share a common underlying mechanism. Our objective was to evaluate whether gestational diabetes influenced the association of prepregnancy Maternal Obesity and risks for CNS birth defects. Methods: This Texas population-based case-control study evaluated births occurring January 1997 through June 2001. Data came from structured telephone interviews. Cases (n = 477) were mothers of offspring with anencephaly (n = 120), spina bifida (n = 184), holoprosencephaly (n = 49), or isolated hydrocephaly (n = 124). Controls (n = 497) were mothers of live infants without abnormalities randomly selected from the same hospitals as cases. Response rates were approximately 60% for both cases and controls. We evaluated Maternal Obesity (body mass index ≥30.0 kg/m 2 ) and risks for CNS birth defects, as well as whether gestational diabetes influenced the risks. Results: After adjusting for Maternal ethnicity, age, education, smoking, alcohol use, and periconceptional vitamin use, obese women had substantially increased risks of delivering offspring with anencephaly (odds ratio = 2.3; 95% confidence interval = 1.2-4.3), spina bifida (2.8; 1.7-4.5), or isolated hydrocephaly (2.7; 1.5-5.0), but not holoprosencephaly (1.4; 0.5-3.8). Odds ratios were higher for the joint effects of Maternal Obesity and gestational diabetes, with evidence for interaction on a multiplicative scale. Conclusions: Maternal Obesity and gestational diabetes may increase the risk of CNS birth defects through shared causal mechanisms.
Sarah R. Mccoski - One of the best experts on this subject based on the ideXlab platform.
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Exposure to Maternal Obesity alters gene expression in the preimplantation ovine conceptus
BMC genomics, 2018Co-Authors: Sarah R. Mccoski, Mccauley T. Vailes, Connor E. Owens, Rebecca R Cockrum, Alan D. EalyAbstract:Background Embryonic and fetal exposure to Maternal Obesity causes several maladaptive morphological and epigenetic changes in exposed offspring. The timing of these events is unclear, but changes can be observed even after a short exposure to Maternal Obesity around the time of conception. The hypothesis of this work is that Maternal Obesity influences the ovine preimplantation conceptus early in pregnancy, and this exposure will affect gene expression in embryonic and extraembryonic tissues.
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Exposure to Maternal Obesity alters gene expression in the preimplantation ovine conceptus
BMC Genomics, 2018Co-Authors: Sarah R. Mccoski, Mccauley T. Vailes, Connor E. Owens, Rebecca R Cockrum, Alan D. EalyAbstract:Background Embryonic and fetal exposure to Maternal Obesity causes several maladaptive morphological and epigenetic changes in exposed offspring. The timing of these events is unclear, but changes can be observed even after a short exposure to Maternal Obesity around the time of conception. The hypothesis of this work is that Maternal Obesity influences the ovine preimplantation conceptus early in pregnancy, and this exposure will affect gene expression in embryonic and extraembryonic tissues. Results Obese and lean ewe groups were established by overfeeding or normal feeding, respectively. Ewes were then bred to genetically similar rams. Conceptuses were collected at day 14 of gestation. Morphological assessments were made, conceptuses were sexed by genomic PCR analysis, and samples underwent RNA-sequencing analysis. While no obvious morphological differences existed between conceptuses, differentially expressed genes (≥ 2-fold; ≥ 0.2 RPKM; ≤ 0.05 FDR) were detected based on Maternal Obesity exposure ( n = 21). Also, differential effects of Maternal Obesity were noted on each conceptus sex ( n = 347). A large portion of differentially expressed genes were associated with embryogenesis and placental development. Conclusions Findings reveal that the preimplantation ovine conceptus genome responds to Maternal Obesity in a sex-dependent manner. The sexual dimorphism in response to the Maternal environment coupled with changes in placental gene expression may explain aberrations in phenotype observed in offspring derived from obese females.
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Maternal Obesity alters the expression of embryonic regulatory transcripts in the preimplantation ovine conceptus.
Reproductive biology, 2018Co-Authors: Sarah R. Mccoski, Mccauley T. Vailes, Rebecca K. Poole, Alan D. EalyAbstract:Abstract The influence of exposure to overfeeding-induced Maternal Obesity around the time of conception on early embryogenesis was examined in the day 14 ovine conceptus. The relative abundance of FGFR2 and DNMT1 was influenced by Maternal Obesity status and conceptus sex, and the abundance of PPARG and PTGS2 transcripts was greater in male conceptuses regardless of the Obesity status of the ewe. These observations demonstrated that short-term exposure to Maternal Obesity impacts early conceptus transcript patterning.
James L Anderson - One of the best experts on this subject based on the ideXlab platform.
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Maternal Obesity gestational diabetes and central nervous system birth defects
Obstetrical & Gynecological Survey, 2005Co-Authors: James L Anderson, Kim D Waller, Mark A Canfield, Gary M Shaw, Margaret L Watkins, Martha M WerlerAbstract:ABSTRACT Several large-scale cohort studies suggest that obese mothers are at increased risk of having infants with neural tube defects and, possibly, other central nervous system (CNS) birth defects. Because Obesity and diabetes share similar metabolic abnormalities, a study was planned to determine whether gestational diabetes influences the association between Maternal Obesity and CNS birth defects. In this population-based case–control study, covering the years 1997 to mid-2000, structured telephone interviews were conducted with mothers of offspring having anencephaly (n = 120), spina bifida (n = 184), holoprosencephaly (n = 49), or isolated hydrocephaly (n = 124). Control women whose infants were neurologically normal were randomly chosen from the same hospitals. Approximately 60% of both cases and control subjects responded. Maternal Obesity was defined as a body mass index of 30 kg/m2 or higher. Pregestational diabetes, both type 1 and type 2, correlated closely with holoprosencephaly (adjusted odds ratio [OR], 47; 95% confidence interval [CI], 9.5–230), and isolated hydrocephaly (OR, 12; 95% CI, 2.9–47). There was no increase in the risk of anencephaly or spina bifida. Gestational diabetes increased only the risk of holoprosencephaly (OR, 2.9; 95% CI, 1.0–8.4). Mothers of infants with anencephaly were less likely than control mothers to have gestational diabetes. Obese mothers were likelier than control subjects to have infants with any of the 4 CNS birth defects. Underweight women were less likely to have an infant with spina bifida. The association between Maternal Obesity and an increased risk of neural tube defects and isolated hydrocephaly held for all ethnic groups. Associations between Maternal Obesity and anencephaly (OR, 2.3; 95% CI, 1.2–4.3), spina bifida (OR, 2.8; 95% CI, 1.7–4.5), and isolated hydrocephaly (OR, 2.7; 95% CI, 1.5–5.0) persisted after adjusting for Maternal age, ethnicity, education, smoking, alcohol use, and periconceptional vitamin use. For both spina bifida and holoprosencephaly, the joint effects of Maternal Obesity and gestational diabetes appeared to be interactive. These findings suggest that gestational diabetes and Maternal Obesity may increase the risk of CNS birth defects through common mechanisms, and they strongly support the need for ways of preventing these conditions.
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Maternal Obesity gestational diabetes and central nervous system birth defects
Epidemiology, 2005Co-Authors: James L Anderson, Kim D Waller, Mark A Canfield, Gary M Shaw, Margaret L Watkins, Martha M WerlerAbstract:Background: Maternal Obesity and diabetes are both associated with increased risk of congenital central nervous system (CNS) malformations in the offspring and may share a common underlying mechanism. Our objective was to evaluate whether gestational diabetes influenced the association of prepregnancy Maternal Obesity and risks for CNS birth defects. Methods: This Texas population-based case-control study evaluated births occurring January 1997 through June 2001. Data came from structured telephone interviews. Cases (n = 477) were mothers of offspring with anencephaly (n = 120), spina bifida (n = 184), holoprosencephaly (n = 49), or isolated hydrocephaly (n = 124). Controls (n = 497) were mothers of live infants without abnormalities randomly selected from the same hospitals as cases. Response rates were approximately 60% for both cases and controls. We evaluated Maternal Obesity (body mass index ≥30.0 kg/m 2 ) and risks for CNS birth defects, as well as whether gestational diabetes influenced the risks. Results: After adjusting for Maternal ethnicity, age, education, smoking, alcohol use, and periconceptional vitamin use, obese women had substantially increased risks of delivering offspring with anencephaly (odds ratio = 2.3; 95% confidence interval = 1.2-4.3), spina bifida (2.8; 1.7-4.5), or isolated hydrocephaly (2.7; 1.5-5.0), but not holoprosencephaly (1.4; 0.5-3.8). Odds ratios were higher for the joint effects of Maternal Obesity and gestational diabetes, with evidence for interaction on a multiplicative scale. Conclusions: Maternal Obesity and gestational diabetes may increase the risk of CNS birth defects through shared causal mechanisms.
Birit F P Broekman - One of the best experts on this subject based on the ideXlab platform.
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influence of Maternal Obesity on the long term health of offspring
The Lancet Diabetes & Endocrinology, 2017Co-Authors: Keith M Godfrey, Rebecca M Reynolds, Susan L Prescott, Moffat Nyirenda, Vincent W V Jaddoe, Johan G Eriksson, Birit F P BroekmanAbstract:In addition to immediate implications for pregnancy complications, increasing evidence implicates Maternal Obesity as a major determinant of offspring health during childhood and later adult life. Observational studies provide evidence for effects of Maternal Obesity on her offspring's risks of Obesity, coronary heart disease, stroke, type 2 diabetes, and asthma. Maternal Obesity could also lead to poorer cognitive performance and increased risk of neurodevelopmental disorders, including cerebral palsy. Preliminary evidence suggests potential implications for immune and infectious-disease-related outcomes. Insights from experimental studies support causal effects of Maternal Obesity on offspring outcomes, which are mediated at least partly through changes in epigenetic processes, such as alterations in DNA methylation, and perhaps through alterations in the gut microbiome. Although the offspring of obese women who lose weight before pregnancy have a reduced risk of Obesity, few controlled intervention studies have been done in which Maternal Obesity is reversed and the consequences for offspring have been examined. Because the long-term effects of Maternal Obesity could have profound public health implications, there is an urgent need for studies on causality, underlying mechanisms, and effective interventions to reverse the epidemic of Obesity in women of childbearing age and to mitigate consequences for offspring.