Academic literature on the topic 'Fetal adiposity'
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Journal articles on the topic "Fetal adiposity"
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Farah, Nadine, Jennifer Hogan, Vicky O'Dwyer, Bernard Stuart, Mairead Kennelly, and Michael J. Turner. "Influence of Maternal Glycemia on Intrauterine Fetal Adiposity Distribution after a Normal Oral Glucose Tolerance Test at 28 Weeks Gestation." Experimental Diabetes Research 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/951203.
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Objective. To examine the relationship between maternal glucose levels and intrauterine fetal adiposity distribution in women with a normal oral glucose tolerance test (OGTT) at 28 weeks gestation.Study Design. We recruited 231 women with a singleton pregnancy. At 28 and 37 weeks gestation, sonographic measurements of fetal body composition were performed. Multiple regression analysis was used to study the influence of different maternal variables on fetal adiposity distribution.Results. Maternal glucose levels correlated with the fetal abdominal subcutaneous tissue measurements (; ) and with birth weight (; ). Maternal glucose levels did not correlate with the fetal mid-thigh muscle thickness and mid-thigh subcutaneous tissue measurements.Conclusion. We found that in nondiabetic women maternal glucose levels not only influence fetal adiposity and birth weight, but also influence the distribution of fetal adiposity. This supports previous evidence that maternal glycemia is a key determinant of intrauterine fetal programming.
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Franca Neto, Antonio H., Melania M. Amorim, Adriana S. Melo, Maria do Carmo P. Lima, Aline Sena, and Lívia Dantas. "Accumulation of Adiposity Fetal During Pregnancy." Obstetrics & Gynecology 127 (May 2016): 132S—133S. http://dx.doi.org/10.1097/01.aog.0000483535.48712.39.
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Franca Neto, Antonio H., Melania M. Amorim, Adriana S. Melo, Aline Sena, Maria do Carmo P. Lima, and Jamila V. Silva. "Thigh Measurement and Adiposity Fetal Accumulation." Obstetrics & Gynecology 127 (May 2016): 149S. http://dx.doi.org/10.1097/01.aog.0000483595.55443.9d.
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Vega-Sanchez, Rodrigo, Hector A. Barajas-Vega, Guadalupe Rozada, Aurora Espejel-Nuñez, Jorge Beltran-Montoya, and Felipe Vadillo-Ortega. "Association between adiposity and inflammatory markers in maternal and fetal blood in a group of Mexican pregnant women." British Journal of Nutrition 104, no. 12 (July 23, 2010): 1735–39. http://dx.doi.org/10.1017/s0007114510002825.
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In the present pilot study, we evaluated the effect of maternal adiposity on the plasma concentration of adipocytokines in pregnant women and their newborns. Twenty patients with term gestations without labour were initially selected by pregestational BMI and then classified into two study groups (n 10 each), according to their median value of adiposity (total body fat). Concentrations of TNF-α, IL-1β, IL-6, leptin and adiponectin in plasma of maternal peripheral blood and fetal cord blood were measured and correlated to maternal adiposity. Maternal adiposity showed a significant negative correlation with fetal adiponectin (r − 0·587, P = 0·01) and IL-6 (r − 0·466, P = 0·05), a significant positive correlation with maternal leptin (r 0·527, P = 0·02) and no correlation with TNF-α or IL-1β. Adiponectin was higher in fetal plasma than in maternal plasma (P = 0·043), but significantly lower in newborns from women with high adiposity than in newborns from women with low adiposity (P = 0·040). Our results suggest that fetuses from obese women may be less able to control inflammation, due to lower circulating anti-inflammatory adipocytokines, which could limit their optimal development or even increase the risk of abortion or preterm labour.
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Sena, Aline Silva Santos, Alex Sandro Rolland de Souza, Vivianne de Oliveira Barros, Maria do Carmo Pinto Lima, Adriana Suely Oliveira Melo, and Melania Maria Ramos de Amorim. "Prenatal factors associated with fetal visceral adiposity." Jornal de Pediatria 96, no. 3 (May 2020): 341–49. http://dx.doi.org/10.1016/j.jped.2018.11.013.
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Sena, Aline Silva Santos, Alex Sandro Rolland de Souza, Vivianne de Oliveira Barros, Maria do Carmo Pinto Lima, Adriana Suely Oliveira Melo, and Melania Maria Ramos de Amorim. "Prenatal factors associated with fetal visceral adiposity." Jornal de Pediatria (Versão em Português) 96, no. 3 (May 2020): 341–49. http://dx.doi.org/10.1016/j.jpedp.2018.11.025.
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Jarvie, Eleanor M., Frances M. Stewart, Jane E. Ramsay, E. Ann Brown, Barbara J. Meyer, Gunilla Olivecrona, Bruce A. Griffin, and Dilys J. Freeman. "Maternal Adipose Tissue Expansion, A Missing Link in the Prediction of Birth Weight Centile." Journal of Clinical Endocrinology & Metabolism 105, no. 3 (December 13, 2019): e814-e825. http://dx.doi.org/10.1210/clinem/dgz248.
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Abstract Context Maternal body mass index (BMI) is associated with increased birth weight but does not explain all the variance in fetal adiposity. Objective To assess the contribution of maternal body fat distribution to offspring birth weight and adiposity. Design Longitudinal study throughout gestation and at delivery. Setting Women recruited at 12 weeks of gestation and followed up at 26 and 36 weeks. Cord blood was collected at delivery. Patients Pregnant women (n = 45) with BMI 18.0 to 46.3 kg/m2 and healthy pregnancy outcome. Methods Maternal first trimester abdominal subcutaneous and visceral adipose tissue thickness (SAT and VAT) was assessed by ultrasound. Main Outcome Measures Maternal body fat distribution, maternal and cord plasma glucose and lipid concentrations, placental weight, birth weight, and fetal adiposity assessed by cord blood leptin. Results VAT was the only anthropometric measure independently associated with birth weight centile (r2 adjusted 15.8%, P = .002). BMI was associated with trimester 2 and trimesters 1 through 3 area under the curve (AUC) glucose and insulin resistance (Homeostatic Model Assessment). SAT alone predicted trimester 2 lipoprotein lipase (LPL) mass (a marker of adipocyte insulin sensitivity) (11.3%, P = .017). VAT was associated with fetal triglyceride (9.3%, P = .047). Placental weight was the only independent predictor of fetal adiposity (48%, P < .001). Maternal trimester 2 and AUC LPL were inversely associated with fetal adiposity (r = -0.69, P = .001 and r = -0.58, P = .006, respectively). Conclusions Maternal VAT provides additional information to BMI for prediction of birth weight. VAT may be a marker of reduced SAT expansion and increased availability of maternal fatty acids for placental transport.
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Luo, Z.-C., A.-M. Nuyt, E. Delvin, F. Audibert, I. Girard, B. Shatenstein, E. Levy, P. Julien, and W. D. Fraser. "Understanding parental anthropometrical, maternal, and fetal metabolic determinants of fetal adiposity." Canadian Journal of Diabetes 35, no. 2 (January 2011): 177. http://dx.doi.org/10.1016/s1499-2671(11)52143-4.
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Edwards, L. J., J. R. McFarlane, K. G. Kauter, and I. C. McMillen. "Impact of periconceptional nutrition on maternal and fetal leptin and fetal adiposity in singleton and twin pregnancies." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 1 (January 2005): R39—R45. http://dx.doi.org/10.1152/ajpregu.00127.2004.
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It has been proposed that maternal nutrient restriction may alter the functional development of the adipocyte and the synthesis and secretion of the adipocyte-derived hormone, leptin, before birth. We have investigated the effects of restricted periconceptional undernutrition and/or restricted gestational nutrition on fetal plasma leptin concentrations and fetal adiposity in late gestation. There was no effect of either restricted periconceptional or gestational nutrition on maternal or fetal plasma leptin concentrations in singleton or twin pregnancies during late gestation. In ewes carrying twins, but not singletons, maternal plasma leptin concentrations in late gestation were directly related to the change in ewe weight that occurred during the 60 days before mating [maternal leptin = 0.9 (change in ewe weight) + 7.8; r = 0.6, P < 0.05]. In twin, but not singleton, pregnancies, there was also a significant relationship between maternal and fetal leptin concentrations (maternal leptin = 0.5 fetal leptin + 4.2, r = 0.63, P < 0.005). The relative mass of perirenal fat was also significantly increased in twin fetal sheep in the control-restricted group (6.0 ± 0.5) compared with the other nutritional groups (control-control: 4.1 ± 0.4; restricted-restricted: 4.4 ± 0.4; restricted-control: 4.3 ± 0.3). In conclusion, the impact of maternal undernutrition on maternal plasma leptin concentrations during late gestation is dependent on fetal number. Furthermore, we have found that there is an increased fetal adiposity in the twins of ewes that experienced restricted nutrition throughout gestation, and this may be important in the programming of postnatal adiposity.
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Wallace, Jacqueline M., John S. Milne, Clare L. Adam, and Raymond P. Aitken. "Impact of donor and recipient adiposity on placental and fetal growth in adolescent sheep." Reproduction 153, no. 4 (April 2017): 381–94. http://dx.doi.org/10.1530/rep-16-0590.
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The influence of maternal obesity during oocyte development and its putative interaction with nutrient reserves at conception on pregnancy outcome were examined in an adolescent sheep model. Donor ewes were nutritionally managed to achieve contrasting adiposity (control (CD)/obese (ObD)) for 6 weeks prior to superovulation and inseminated by a non-obese sire. Morulae from 6 CD and 7 ObD were transferred in singleton into adolescent recipients of identical age but differing adiposity, classified as relatively fat or thin respectively. Thereafter, all were overnourished to promote rapid growth/adiposity (2 × 2 design, 13/14 pregnancies/group). A fifth recipient group of intermediate adiposity received embryos from another 5 CD, was offered a moderate intake to maintain adiposity throughout gestation and acted as controls for normal pregnancy outcome (optimally treated control (OTC), 19 pregnancies). Donor obesity did not influence ovulation, fertilisation or recovery rates or impact embryo morphology. Gestation length and colostrum yield were unaffected by donor or recipient adiposity and were reduced relative to OTC. Total fetal cotyledon and lamb birth weights were independent of initial donor adiposity but reduced in relatively thin vs relatively fat recipients and lower than those in the OTC group. In spite of high placental efficiency, the incidence of fetal growth restriction was greatest in the thin recipients. Thus, maternal adiposity at conception, but not pre-conception maternal obesity, modestly influences the feto-placental growth trajectory, whereas comparison with the OTC indicates that high gestational intakes to promote rapid maternal growth remain the dominant negative influence on pregnancy outcome in young adolescents. These findings inform dietary advice for pregnant adolescent girls.
Dissertations / Theses on the topic "Fetal adiposity"
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Solé, Navais Pol. "Prenatal one carbon metabolism and in utero programming of growth and adiposity in the offspringPrenatal one carbon metabolism and in utero programming of growth and adiposity in the offspring." Doctoral thesis, Universitat Rovira i Virgili, 2016. http://hdl.handle.net/10803/401551.
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El metabolisme monocarbonat influeix positivament la salut en estadis primerencs i tardans de la vida (e.g. reducció en la prevalença de defectes del tub neural i la mort per accidents vasculars cerebrals després de la fortificació amb àcid fòlic). Tot i això, es desconeixen els efectes que el metabolisme monocarbonat in utero pot tenir sobre el creixement postnatal. S’han atribuït efectes adversos a estats elevats de folat. L’objectiu era avaluar les interaccions entre el folat i cobalamina prenatals i els seus efectes durant l’embaràs i sobre el creixement i adipositat en la descendència. Es van estudiar 563 dones del Reus-Tarragona Birth Cohort durant l’embaràs i 162 nens fins als 7.5 anys. L’estat en folats no va modificar l’associació entre l’estat inadequat en cobalamin i marcadors metabòlics i hematològics durant l’embaràs. Un estat inadequat a l’inici de l’embaràs en folat eritrocitàri, cobalamina o tHcy es va associar amb menor alçada en la descendència. Un estat inadequat en holoTC es va associar amb major IMC en la descendència. Els polimorfismes materns MTHFR 677C>T i TCN2 776C>T es van associar amb major i menor IMC i alçada en la descendència des del naixement fins als 7.5 anys respectivament. El polimorfisme MTRR 66A>G del nen es relacionava amb menor alçada i pes. Aquests resultats avalen la seguretat d’elevades concentracions de folat plasmàtic i sustenten el paper del metabolisme monocarbonat prenatal en el creixement i adipositat postnatals.El metabolismo monocarbonado influye positivamente la salud en estadios tempranos y tardíos de la vida (e.g. reducción en la prevalencia de defectos del tubo neural y la muerte por accidente vascular cerebral después de la fortificación con ácido fólico). Se desconocen los efectos del metabolismo monocarbonado in utero en el crecimiento postnatal. Se han atribuido efectos adversos a un estado elevado en folato. El objetivo fue evaluar las interacciones entre el folato y cobalamina prenatales i sus efectos durante el embarazo y sobre el crecimiento y adiposidad en la progenie. Se estudiaron 563 mujeres del Reus-Tarragona Birth Cohort durante el embarazo y 162 descendientes hasta los 7.5 años de edad. Un estado elevado en folatos no modificó la asociación entre concentraciones inadecuadas de cobalamina y sus marcadores metabólicos o hematológicos durante el embarazo. Un estado inadecuado al inicio del embarazo en folato eritrocitario, cobalamina o tHcy al inicio del embarazo se asoció con menor estatura en la descendencia. Un estado inadecuado en holoTC se asoció con mayor IMC en los descendientes. Los polimorfismos maternos MTHFR 677C>T y TCN2 776C>T se asociaron con mayor y menor IMC y estatura desde el nacimiento hasta la infancia respectivamente. El polimorfismo MTRR 66A>G del niño se relacionaba con menor talla y peso. Estos resultados avalan la seguridad de concentraciones elevadas en folato plasmático y sostienen el papel del metabolismo monocarbonado prenatal en el crecimiento y adiposidad postnatales.
One carbon metabolism positively influences health in early and late stages of life (e.g. folic acid fortification reduced neural tube defect prevalence, homocysteine in adults and possiblystroke mortality). Whether the effects of in utero one carbon metabolism affect postnatal growth is unknown. Harmful effects of elevated folate status have been reported. We evaluated the interactions between prenatal folate and cobalamin and their effects during pregnancy and on offspring growth and adiposity at mid-childhood. 563 women from the Reus-Tarragona Birth Cohort were followed-up throughout pregnancy and 162 of their offspring until mid-childhood, when growth and adiposity were measured. Folate status did not modify the association between inadequate cobalamin and its metabolic or haematological indicators. Early pregnancy inadequate RBC folate, cobalamin or tHcy were associated with lower offspring height. Inadequate holoTC was also associated with higher offspring BMI. Maternal MTHFR 677C>T and TCN2 776C>T genetic variants were associated with higher and lower offspring BMI and height from birth to mid-childhood, respectively. Child MTRR 66A>G was associated with lower linear and ponderal growth. This endorses the safety of elevated folate status, and supports a role for prenatal one carbon metabolism on postnatal growth and adiposity.
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Ferraro, Zachary Michael. "An Examination of Maternal Contributors and Potential Modifiers of Fetal Growth in Pregnancy." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/22817.
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A greater understanding of critical periods of body weight regulation, including pregnancy, may aid in efforts to optimize weight management strategies for the mother and her baby. The gestational period has been implicated to play, in the child, a vital role in the developmental origins of obesity and other cardiometabolic diseases later in life. Therefore, we initially examined existing literature on the role of maternal obesity and its link to pediatric obesity and documented the known underlying physiological mechanisms responsible for this relationship while suggesting potential intervention targets that may improve maternal-fetal outcomes. In a second paper, we aimed to quantify maternal predictors of large for gestational age (LGA) neonates in the Ottawa and Kingston (OaK) birth cohort with specific hypotheses verifying the independent contribution of maternal prepregnancy body mass index (BMI) and excessive gestational weight gain (GWG) to fetal overgrowth. This paper also highlights the clinical utility of the revised 2009 Institute of Medicine GWG guidelines and discusses the potential role of physiological factors underlying the observed associations between BMI, excessive GWG and LGA neonates. As a follow-up to our population-level analysis (i.e., OAK cohort), papers three and four highlight how the insulin-like growth factor (IGF) axis, a vital regulator of growth and development, may be compromised at the molecular level in cases of maternal obesity (paper 3) and excessive GWG (paper 4). In paper 3 we show that maternal obesity is associated with attenuated expression of IGF binding protein-4 (IGFBP4) in umbilical cord blood and discuss how this may preferentially promote fetal adipogenesis. The effects of excessive GWG on IGF axis protein expression are addressed in paper four where we show that excessive weight gain during pregnancy is associated with increased expression of IGFBP3 in maternal circulation in normoglycemic term pregnancies. In this paper we discuss the potential inhibitory role of IGFBP3 on adipogenesis and how it relates to glucose intolerance during pregnancy. Recognizing that both obesity and excessive GWG can alter physiological processes in mother and her baby, appropriate evidence-based interventions are warranted to best optimize outcomes. In paper five, we discuss the results of a study which sought to assess patient information channels and knowledge of nutrition and physical activity during pregnancy with the intent that these findings be applied to best design efficacious strategies that cater to the needs of our target group of pregnant women. In our analysis we show that the majority of pregnant women studied would be willing to participate in a lifestyle intervention for their own personal health and that of their child. Of great interest was the observation that most women were not informed of the importance of pregnancy-specific energy intake, or made aware of their own healthy GWG targets. Additionally, many of the respondents reported receiving no information pertaining to appropriate physical activity recommendations; despite the fact that the vast majority of participants consider this lifestyle modality to be safe during their pregnancy. Finally in paper six, we build on the results of our previous work and evaluate the risks and benefits of physical activity during pregnancy on maternal-fetal outcomes through a review of the literature and note that engaging in non-sedentary pursuits during gestation may aid in maternal weight regulation, protect against metabolic disorders and optimize neonatal birth weight and body composition. Overall, the collective nature of the papers presented in this dissertation provides qualitative and quantitative evidence to support not only the complexity of body weight regulation in the mother and her baby, but also highlights potential avenues for intervention that may improve maternal-fetal outcomes during this critical period.
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Nasr, Elizabeth Maria Bismarck. "Excesso de peso corporal na adolescência segundo períodos críticos para a gênese da obesidade durante a infância." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/6/6138/tde-31012013-085539/.
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Introdução: Considerando-se a dificuldade e o elevado custo para o tratamento da obesidade, e seu papel como fator de risco para diversas patologias, sua prevenção mostra-se fundamental, por este motivo, a identificação precoce de fatores de risco evitáveis, como a inadequação do estado nutricional em períodos críticos para a gênese da obesidade, representa um interessante campo para investigação científica. Objetivo: Verificar a relação entre o excesso de peso corporal em adolescentes segundo estado nutricional ao nascer e excesso de peso durante o primeiro ano de vida e no período de repleção da adiposidade. Método: Participaram deste estudo alunos de ambos os sexos matriculados nos quintos e sextos anos de Unidades Escolares no Município de São José dos Campos-SP. A coleta de dados ocorreu em três etapas, a primeira consistiu na avaliação nutricional durante a adolescência, considerando-se as medidas de índice de massa corporal (IMC), circunferências abdominal e do braço e soma das pregas cutâneas triciptal e subescapular. Na segunda etapa foram coletadas informações referentes à escolaridade materna, aleitamento materno e estado nutricional ao nascer por meio de questionário respondido pelos pais. As crianças foram classificadas segundo os índices peso ao nascer por idade gestacional, índice ponderal ao nascer e peso ao nascer. Na última etapa foram obtidas informações de peso e estatura durante a infância nos prontuários de atendimento das Unidades Básicas de Saúde (UBS) do Município. Realizou-se análise de regressão logística para verificar associação entre excesso de peso aos 10 anos de idade, considerada variável dependente e, como variáveis independentes, estado nutricional ao nascer, excesso de peso corporal no primeiro ano de vida e no período de repleção da adiposidade (entre os 5 e 7 anos de idade). As análises foram ajustadas para demais variáveis. Resultados: Os estudantes apresentaram média (desvio-padrão) de 131,3 meses (10,99) de idade. Verificou-se elevada correlação entre o peso e comprimento ao nascer informado pelos responsáveis e registrado no prontuário das UBSs (coeficiente de correlação: 0,95 e 0,98, respectivamente). Com relação ao estado nutricional ao nascer, observou-se que o elevado peso ao nascer e o peso ao nascer pequeno para idade gestacional associaram-se ao excesso de peso corporal no início da adolescência. Foi identificado limiar de associação entre excesso de peso corporal no primeiro ano de vida e aos 10 anos de idade. Também foi encontrada associação entre excesso de peso corporal na adolescência e no período de repleção da adiposidade. Conclusão: Os achados mostram consistência com a hipótese de que períodos críticos do crescimento acarretariam em maior predisposição ao excesso de gordura corporal, identificada no presente estudo no início da adolescênciaIntroduction: Considering that obesity is a major risk for many diseases as well as the difficulties and elevated costs for its treatment, its prevention and the identification of early avoidable health risks, such as nutritional status in critical periods of life, represent important aspects for scientific investigation. Objective: Verify the relationship between excessive body weight during adolescence according to birth nutrition status and excessive body weight during the first year of life and at the period of adiposity rebound. Method: This study was conducted with schoolchildren of both sexes, enrolled in Public Schools in São José dos Campos - SP (SJC-SP). The data was collected in 3 phases, the first consisted of collecting anthropometric information during adolescence, considering body mass index (BMI), arm and abdominal circumferences and the sum of skin fold thickness (triceps and sub scapular). Information about mother´s education, breastfeeding and birth nutritional status was collected in the second phase through a survey which the parents answered. The children were classified according to birth weight for gestational age, ponderal index and birth weight. In the last phase, information about nutritional status during infancy was obtained from medical registers of primary health units in the city. Logistical regression analyses were made to investigate the association between excessive body weight at 10 years of age, considered as dependent variable and, as independent variables, the nutritional status at time of birth, the first year of age and during the period of adiposity rebound (between 5 and 7 years of age). The analyses were adjusted by other variables. Results: The students presented a mean of 131.3 months of age (10.99). An elevated correlation was observed between parents information about birth weight and length and the information registered at the medical documents of primary health units in the city (Correlation coefficient: 0.95 and 0.98, for weight and for length, respectively). An association between elevated birth weight and birth weight small for gestational age and excessive body weight during adolescence was observed. A weak association between excessive body weight during the first year of life and at 10 years of age was identified. It was also verified association in relation to adiposity during the period of adiposity rebound and excessive weight at 10 years of age. Conclusion: These results show consistency in the hypothesis that the critical period for growth development could predispose to future obesity, identified in the present study during early adolescence
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Tavares, Neuziane Kloos Amorim. "Avaliação das consequências da limitação do tamanho da prole de ratos Wistar ao nascimento sobre seu desenvolvimento ponderal e características morfofuncionais na idade adulta." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-27092013-155436/.
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Durante a vida intrauterina, o desenvolvimento do embrião e do feto é suscetível a mudanças ambientais que podem alterar o fenótipo do indivíduo na vida pós-natal. Eventos que ocorrem durante períodos críticos de rápida divisão celular, nos quais são formados os diversos órgãos e tecidos, podem alterar a estrutura e função de sistemas orgânicos gerando consequências precoces (baixo peso ao nascimento) e tardias (doenças na vida adulta). Os protocolos experimentais da maior parte dos estudos sobre a programação fetal reduz o tamanho da ninhada logo após o nascimento. Essa abordagem dificulta a interpretação e reprodutibilidade dos resultados observados. O objetivo deste estudo foi determinar se a pressão sanguínea, o metabolismo de carboidratos e gasto energético em proles adultas é influenciado pelo tamanho da ninhada. Ratas Wistar foram alimentadas com ração padrão ad libitum e foram acasaladas com ratos machos com 12 semanas de idade. Após o nascimento, a prole foi dividida em três grupos: tamanho da ninhada sem redução (Gc), proles reduzido a oito filhotes (G8) e proles reduzidos a quatro filhotes (G4). Ao fim de 12 semanas de idade, o peso corporal, pressão arterial, consumo de ração, glicemia, insulina, colesterol e triacilgliceróis, massa de tecido adiposo marrom, índice de adiposidade, massa renal e cardíaca foram determinados. O peso corporal, índice de adiposidade, glicemia, nível de insulina e índice HOMA foram maiores em machos e fêmeas no grupo G4 do que nos grupos G8 e Gc. No entanto, o consumo de ração foi menor no grupo G4. A pressão arterial foi maior no grupo Gc em machos e fêmeas. Em resumo, a redução do tamanho da ninhada está relacionada com a obesidade, resistência à insulina e possíveis alterações no gasto energético na prole adultaDuring intrauterine life, the developing fetus is susceptible to environmental changes that can alter the phenotype of the individual in postnatal life. This phenomenon is called fetal programming. Events that occur during critical periods of rapid cell division may alter the structure and function of organ systems, resulting in consequences both early (low birth weight) and late (diseases in adulthood) in life. The experimental protocols of most of the studies on fetal programming involve a reduction in litter size soon after birth. This approach hampers the interpretation and reproducibility of the observed results. The purpose of this investigation was to determine if blood pressure, carbohydrate metabolism and energy expenditure in adult offspring are influenced by litter size. Female Wistar rats were fed standard rat chow ad libitum and were mated with male rats at 12 weeks of age. After birth, the offspring were divided into three groups: unchanged litter size (GU), culled to eight neonates (G8) and culled to four neonates (G4). At 12 weeks of age, the body weight; blood pressure; food intake; glucose, insulin, cholesterol and triacylglycerol levels; brown adipose tissue mass; adiposity index; renal mass; and cardiac mass were determined. The body weight, adiposity index, glucose level, insulin level and HOMA index were higher in males and females in the G4 group than in the G8 and GU groups. However, food consumption was lower in G4 males. The blood pressure was higher in the GU group. In summary, a small litter size is related to obesity, possible alterations in energy expenditure and insulin resistance in adult offspring
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Ballesteros, Pérez Mònica. "Multímeros de la adiponectina en la diabetes gestacional: relación con parámetros maternos y repercusión en el crecimiento fetal." Doctoral thesis, Universitat Rovira i Virgili, 2011. http://hdl.handle.net/10803/63591.
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El tejido adiposo juega un activo papel en la homeostasis metabólica. Sus funciones son mediadas por unos factores secretados por los adipocitos conocidos como adipocitoquinas.
La adiponectina es una adipocitoquina producida en los adultos en el tejido graso y en los fetos en varios tejidos fetales. Presente en la circulación sanguínea en forma de multímeros de diferentes pesos moleculares con diferentes implicaciones funcionales.
Se encuentra inversamente relacionado con los niveles de insulinoresistencia, que se incrementan en la gestación, agravándose en la diabetes gestacional (DMG), entidad asociada a macrosomia fetal, hemos postulado que la cantidad y distribución de sus multímeros adiponectina tanto maternos como fetales, pueden ser uno de los factores implicados en la regulación del crecimiento fetal y la adiposidad neonatal.
Postulamos sobre una correlación de los niveles de adiponectina materna y fetal.
También hemos valorado nuevas fórmulas de estimación de peso ecográficas en tres dimensiones.Adipose tissue plays an active role in metabolic homeostasis. Its functions are mediated by factors secreted by adipocytes known as adipocytokines. Adiponectin is an adipocytokine produced in the adult fat tissue and fetuses in various fetal tissues. Present in the bloodstream in the form of multimers of different molecular weights with different functional implications. Is inversely related to levels of insulin resistance, which increased during pregnancy, gestational diabetes to worsen in the (DMG), an entity associated with fetal macrosomia, we postulate that the quantity and distribution of adiponectin multimers both maternal and fetal, can be one of the factors involved in regulating fetal growth and neonatal adiposity. We postulate a correlation of levels of maternal and fetal adiponectin. We also evaluated new methods of weight estimation in three-dimensional ultrasound.
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Grothe, Jon-Frederic [Verfasser], Jörg [Gutachter] Dötsch, and Christhardt [Gutachter] Köhler. "Plazentare Dysfunktion bei maternaler Adipositas : Auswirkungen auf die fetale und plazentare Entwicklung / Jon-Frederic Grothe ; Gutachter: Jörg Dötsch, Christhardt Köhler." Köln : Deutsche Zentralbibliothek für Medizin, 2020. http://d-nb.info/1223658457/34.
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Poprzeczny, Amanda Josephine. "Maternal Overweight and Obesity: Effect on Fetal Growth and Adiposity." Thesis, 2022. https://hdl.handle.net/2440/136348.
Full textAbstract:
Background: Maternal overweight and obesity are associated with well-documented maternal and infant risks, including high infant birth weight and delivery of an infant large for gestational age. However, less is known about the impact of maternal BMI on fetal growth and adiposity, and growth and adiposity trajectories. There is limited information regarding the effects of antenatal interventions to limit gestational weight gain on fetal growth and adiposity. Methods: This thesis examines the effect of maternal BMI on fetal growth and adiposity, antenatal contributors to fetal growth and adiposity, and the effect of antenatal interventions on fetal growth and adiposity using data from a set of three harmonised randomised trials conducted between June 2008 and April 2017. Women were invited to attend for a research ultrasound at 28 and 36 weeks of gestation, where fetal biometry and adiposity measures were obtained. The analyses reported in this thesis investigate: 1. The effect of maternal BMI, across the BMI spectrum, on fetal growth and adiposity; 2. Whether this effect is mediated by (diagnosed and treated) GDM; 3. How fetal growth and adiposity is altered among infants born LGA; and 4. The effect of antenatal interventions to limit gestational weight gain on fetal growth and adiposity. Results: The analyses reported in this thesis find that: 1. Maternal BMI exerts a strong, continuous positive effect on fetal growth and adiposity measures, from as early as 20 weeks’ gestation; 2. Among women who are overweight or obese, there is no evidence of a mediated effect by diagnosed and treated GDM; 3. Infants born LGA demonstrate larger fetal biometry and adiposity measures from as early as 20 weeks’ gestation; and 4. There is no evidence that the antenatal interventions investigated in this thesis are sufficient to alter fetal growth and adiposity. Conclusions: Overall, the findings presented in this thesis suggest fetal growth patterns are determined early in pregnancy, and any antenatal interventions to prevent the effects of maternal overweight and obesity on fetal growth will need to be commenced earlier in pregnancy, or prior to conception, to be effective in preventing the intergenerational inheritance of overweight and obesity.Thesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 2022
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Krafczyk, Bianca [Verfasser]. "Maternale und fetale, neonatale Risiken der Adipositas in der Schwangerschaft : Analyse eines Schwangerenkollektivs mit 508.926 Einlingsgeburten der Jahre 1998 - 2000 der Bundesrepublik Deutschland / vorgelegt von Bianca Krafczyk." 2008. http://d-nb.info/995099642/34.
Full textBooks on the topic "Fetal adiposity"
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Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Macronutrients and fibre requirements during pregnancy. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0004.
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In this chapter, the impact of varying intakes of protein, carbohydrate and lipids, which are the key nutrients that contribute to calorie intake, is examined. Fibre is also an important food component that needs to be considered. The maternal macronutrient profile can influence embryonic and fetal development. For instance, both low and excessively high protein intakes during pregnancy are associated with restricted growth, increased adiposity, and impaired glucose tolerance. High-fat maternal diets can significantly increase the susceptibility to diet-induced obesity and percentage total body fat in offspring, although types of fats need to be considered, as intake of polyunsaturated fatty acids is important for fetal development. The type and content of carbohydrate (high- vs low-glycaemic sources) in the maternal diet influences blood glucose concentration, which has a direct effect on fetal glucose levels and metabolism.
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Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Polyunsaturated fatty acids in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0005.
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Evidence for the importance of the long-chain omega-3 polyunsaturated fatty acids in fetal and infant development is growing, as is interest in what constitutes an appropriate intake from sources such as oily fish or dietary supplements for pregnant women and/or infants. Polyunsaturated fatty acids have been implicated in maternal mental health and aspects of infant development, including cognitive and visual function, adiposity, and allergy. Western diets have become imbalanced with regard to the ratio of omega-6:omega-3 fatty acids, and recommendations to correct this imbalance include increasing the maternal intake of oily fish. However, this recommendation needs to be evaluated in light of the increased risk of exposure to contaminants such as mercury. Vegetable oils and cereals are important sources of polyunsaturated fatty acids for vegetarians.
Book chapters on the topic "Fetal adiposity"
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Khanal, Prabhat, and Mette Olaf Nielsen. "Maternal Undernutrition and Visceral Adiposity." In Diet, Nutrition, and Fetal Programming, 91–105. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-60289-9_8.
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Schäfer-Graf, Ute. "Abnormer Glukosemetabolismus und Adipositas: fetale und neonatale Kurz- und Langzeitrisiken und ihr klinisches Management." In Praxisbuch Adipositas in der Geburtshilfe, 145–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 2022. http://dx.doi.org/10.1007/978-3-662-61906-3_7.
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Low, Felicia, Peter Gluckman, and Mark Hanson. "Fetal and Early Postnatal Life Determinants of Adiposity." In Handbook of Obesity, 127–36. CRC Press, 2014. http://dx.doi.org/10.1201/b16473-14.
Full textConference papers on the topic "Fetal adiposity"
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Bukowski, Michael, Brij Singh, James Roemmich, and Kate Larson. "Lipidomic analysis of TRPC1 Ca2+-permeable channel-knock out mouse demonstrates a vital role in placental tissue sphingolipid and triacylglycerol homeostasis under high-fat diet." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/tjdt4839.
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Placental function including oxygen delivery and nutrient transport are critical determinants of fetal growth, moderating the risks of obesity and metabolic diseases later in life. Previously, we demonstrated in a mouse model that parental diet and exercise play important roles in placental lipid content and inflammation. Transient receptor potential canonical channel 1 (TRPC1) is a Ca2+-permeable integral membrane protein. We have demonstrated that TRPC1 increases total body adiposity in mice by decreasing the efficacy of exercise to limit adipose accumulation under a high fat (HF) diet. Importantly, intracellular calcium may regulate total body adiposity and increased total body adiposity could promote placental lipid accumulation. Similarly, intracellular calcium regulates membrane lipid content via the activation of the protein kinase C. Membrane lipids such as sphingomyelin are key regulators of cell signaling. Maternal HF diets increase placental tissue lipid concentrations resulting in compromised nutrient transport to fetus. However, the specific lipid species that accumulate due to the absence of the placental TRPC1 gene under maternal HF diet feeding is not yet known. We hypothesized that placental tissue response to a maternal HF diet is disrupted in TRPC1 mice fed a maternal HF diet resulting in greater cellular sphingomyelin concentrations. Results showed placentae from TRPC1 KO mice fed high fat diet (45% en, HF) had increased sphingomyelin concentrations compared to control diet (16% en, NF). Placentae from WT mice fed HF diet exhibited diet-dependent increases in ceramide concentration with no concomitant increase in sphingomyelins compared to NF fed WT mice. Additionally, 11 placental triacylglycerol (TAG) species were different based on diet, 16 based on genotype, and 5 were affected by both diet and genotype. These results suggest that during a HF diet, loss of TRPC1 function reduces placental sphingomyelin hydrolysis into ceramide and that placental TAG concentrations respond in diet- and genotype-dependent manner.