Log in

Relevant bibliographies by topics / Intrauterine programming

Academic literature on the topic 'Intrauterine programming'

Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Journal articles
Dissertations / Theses
Books
Book chapters

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Intrauterine programming.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Intrauterine programming"

1

Lister, Rolanda. "Intrauterine Programming of Diabetes Induced Cardiac Embryopathy." Diabetes & Obesity International Journal 4, no. 3 (2019): 1–14. http://dx.doi.org/10.23880/doij-16000202.

Full text

Abstract:

Background: Maternal hyperglycemia is a well-recognized risk factor for fetal congenital heart disease. However, the underlying cellular and molecular mechanisms are not well characterized. We hypothesize that maternal hyperglycemia leading to congenital heart are linked to abnormal DNA methylation and mRNA expression at cardiac specific loci. Methods: Hyperglycemia was induced in normal 8-week old CD-1 female mice with a one-time intraperitoneal injection of 150 mg/kg of streptozotocin (STZ) 2 weeks prior to mating. Histological analysis of fetal cardiac morphology was evaluated for malformations on embryonic day (E) 16.5 of control pups and pups exposed to maternal hyperglycemia. We used a massively-parallel sequencing-based methylation sensitive restriction based assay to examine genome-wide cytosine methylation levels at >1.65 million loci in neonatal hearts on post-natal (P) day 0. Functional validation was performed with real time quantitative polymerase chain reaction (RT-qPCR). Results: Cardiac structural defects occurred in 28% of the pups (n=12/45) of hyperglycemic dams versus 7% (n=4/61) of controls. Notable phenotypes were hypoplastic left or right ventricle, double outlet right ventricle, ventricular septal defect, and left ventricular outflow tract obstruction. A 10-fold increase in DNA methylation of gene promoter regions was seen in many cardiac important genes in the experimental versus control P0 neonates and have corresponding decreases in gene expression in 21/32 genes functionally validated. Conclusion: Maternal hyperglycemia alters DNA methylation and mRNA expression of some cardiac genes during heart development. Quantitative, genome-wide assessment of cytosine methylation can be used as a discovery platform to gain insight into the mechanisms of hyperglycemia-induced cardiac anomalies.

APA, Harvard, Vancouver, ISO, and other styles

2

Fernandez‐Capetillo, Oscar. "Intrauterine programming of ageing." EMBO reports 11, no. 1 (December 11, 2009): 32–36. http://dx.doi.org/10.1038/embor.2009.262.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Fowden, A. L., and A. J. Forhead. "Endocrine mechanisms of intrauterine programming." Reproduction 127, no. 5 (May 2004): 515–26. http://dx.doi.org/10.1530/rep.1.00033.

Full text

Abstract:

Epidemiological findings and experimental studies in animals have shown that individual tissues and whole organ systems can be programmedin uteroduring critical periods of development with adverse consequences for their function in later life. Detailed morphometric analyses of the data have shown that certain patterns of intrauterine growth, particularly growth retardation, can be related to specific postnatal outcomes. Since hormones regulate fetal growth and the development of individual fetal tissues, they have a central role in intrauterine programming. Hormones such as insulin, insulin-like growth factors, thyroxine and the glucocorticoids act as nutritional and maturational signals and adapt fetal development to prevailing intrauterine conditions, thereby maximizing the chances of survival bothin uteroand at birth. However, these adaptations may have long-term sequelae. Of the hormones known to control fetal development, it is the glucocorticoids that are most likely to cause tissue programmingin utero. They are growth inhibitory and affect the development of all the tissues and organ systems most at risk of postnatal pathophysiology when fetal growth is impaired. Their concentrationsin uteroare also elevated by all the nutritional and other challenges known to have programming effects. Glucocorticoids act at cellular and molecular levels to alter cell function by changing the expression of receptors, enzymes, ion channels and transporters. They also alter various growth factors, cytoarchitectural proteins, binding proteins and components of the intracellular signalling pathways. Glucocorticoids act, directly, on genes and, indirectly, through changes in the bioavailability of other hormones. These glucocorticoid-induced endocrine changes may be transient or persist into postnatal life with consequences for tissue growth and development both before and after birth. In the long term, prenatal glucocorticoid exposure can permanently reset endocrine systems, such as the somatotrophic and hypothalamic–pituitary–adrenal axes, which, in turn, may contribute to the pathogenesis of adult disease. Endocrine changes may, therefore, be both the cause and the consequence of intrauterine programming.

APA, Harvard, Vancouver, ISO, and other styles

4

Ige, S. F., R. E. Akhigbe, and O. O. Akinsemola. "Intrauterine Programming and Postnatal Hypertension." Research Journal of Obstetrics and Gynecology 4, no. 1 (January 1, 2011): 1–27. http://dx.doi.org/10.3923/rjog.2011.1.27.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Barker, David J. P. "Intrauterine programming of adult disease." Molecular Medicine Today 1, no. 9 (December 1995): 418–23. http://dx.doi.org/10.1016/s1357-4310(95)90793-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Fowden, A. L., O. A. Valenzuela, O. R. Vaughan, J. K. Jellyman, and A. J. Forhead. "Glucocorticoid programming of intrauterine development." Domestic Animal Endocrinology 56 (July 2016): S121—S132. http://dx.doi.org/10.1016/j.domaniend.2016.02.014.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Fowden, A. L., A. J. Forhead, P. M. Coan, and G. J. Burton. "The Placenta and Intrauterine Programming." Journal of Neuroendocrinology 20, no. 4 (April 2008): 439–50. http://dx.doi.org/10.1111/j.1365-2826.2008.01663.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Remacle, C., O. Dumortier, V. Bol, K. Goosse, P. Romanus, N. Theys, T. Bouckenooghe, and B. Reusens. "Intrauterine programming of the endocrine pancreas." Diabetes, Obesity and Metabolism 9, s2 (November 2007): 196–209. http://dx.doi.org/10.1111/j.1463-1326.2007.00790.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Gale, C. R. "Intrauterine Programming of Adult Body Composition." Journal of Clinical Endocrinology & Metabolism 86, no. 1 (January 1, 2001): 267–72. http://dx.doi.org/10.1210/jc.86.1.267.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Gale, Catharine R., Christopher N. Martyn, Samantha Kellingray, Richard Eastell, and Cyrus Cooper. "Intrauterine Programming of Adult Body Composition1." Journal of Clinical Endocrinology & Metabolism 86, no. 1 (January 2001): 267–72. http://dx.doi.org/10.1210/jcem.86.1.7155.

Full text

APA, Harvard, Vancouver, ISO, and other styles

More sources

Dissertations / Theses on the topic "Intrauterine programming"

1

Franko, Kathryn Lynette. "Regulation and intrauterine programming of glucogenic capacity." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.613228.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Crispi, Brillas Fàtima. "Fetal programming of cardiovascular dysfunction in intrauterine growth restriction." Doctoral thesis, Universitat de Barcelona, 2009. http://hdl.handle.net/10803/2276.

Full text

Abstract:

BACKGROUND

Fetal growth restriction (FGR), with a prevalence of 5-10% in newborns, is associated with increased cardiovascular mortality in adulthood, but the pathophysiological links of this relationship are only partially understood. The main hypothesis of this thesis was that FGR induces primary cardiac dysfunction and remodelling in utero that persists postnatally and leads to increased cardiovascular risk in adulthood.

METHODS

Cardiovascular function was assessed in a cohort of FGR fetuses and correlated to the severity stages of FGR, presence of preeclampsia and also perinatal data in order to evaluate its potential utility in the clinical management of these fetuses. Finally, cardiac and vascular function was also assessed in childhood.

RESULTS

In utero, FGR fetuses showed signs of subclinical cardiac dysfunction measured by echocardiography (increased E/A ratios and isovolumic times with normal cardiac output) from early stages. Cardiac dysfunction deteriorated further with the progression of fetal compromise, together with the appearance of biochemical signs of cell damage (increased heart-fatty acid binding protein concentrations in cord blood). Preeclampsia per se was not associated to cardiac function in FGR fetuses. Cardiac function parameters, such as ductus venosus and myocardial performance index, were independently associated with perinatal death in preterm FGR. Therefore, a combination cardiac parameters may be useful in the clinical management of preterm FGR by stratifying the estimated probability of death. Children with FGR showed changes in cardiac shape (more globular morphology), subclinical cardiac dysfunction (increased heart rate and reduced stroke volume and myocardial peak velocities) and vascular remodelling (increased blood pressure and carotid intima-media thickness).

CONCLUSIONS

FGR present cardiovascular dysfunction in utero that persists postnatlly. These findings suggest that fetal growth restriction induces primary cardiac changes which could explain the increased predisposition to cardiovascular disease in adult life. Given its high prevalence in the general population, this might have to be taken into account in assessing cardiovascular risk factors and treatment.
INTRODUCCIÓN

El retaso de crecimiento intrauterino (CIR), con una prevalencia del 5-10% de los recién nacidos, se asocial a un aumento de la mortalidad cardiovascular en vida adulta, pero la fisiopatología de esta correlación aun es incierta. La principal hipótesis de esta tesis fue que el CIR induce una disfunción y remodelado cardiovascular primario in útero que después persiste en vida postnatal y condiciona un aumento del riesgo cardiovascular en vida adulta.

MÉTODOS

En una cohorte de fetos CIR se evaluó la función cardiovascular y se correlacionó con el grado de severidad del CIR, la presencia de preeclampsia y también los resultados perinatales, para poder evaluar su potencial utilidad en el manejo clínico de estos fetos. Finalmente, la función cardiovascular también fue evaluada postnatalmente.

RESULTADOS

En útero, los fetos CIR mostraron signos de disfunción cardiaca subclínica medida mediante eco cardiografía (aumento de los ratios E/A i tiempos isovolumétricos, con gasto cardíaco normal) des de estadios iniciales de severidad. La función cardiaca mostró un deterioro progresivo con el aumento de severidad del CIR, a la vez que aparecieron signos bioquímicos de daño miocárdico en estadios finales de deterioro (aumento de los niveles de heart-fatty acid binding proteins en sangre de cordón). La preeclampsia per se no mostró asociación con el grado de disfunción cardiaca. Algunos parámetros de función cardiaca fetal, como el ductus venoso y el índice de rendimiento miocárdico, mostraron una asociación independiente con la mortalidad perinatal en los casos de CIR pretérmino. A nivel postnatal, los niños con antecedente de CIR mostraron cambios en la morfología cardiaca (más globular), disfunción cardiaca subclínica (aumento de la frecuencia cardiaca, y reducción del volumen de eyección y velocidades miocárdicas) y remodelación vascular (aumento de la presión arterial y grosor de las carótidas).

CONCLUSIONES

Los casos de CIR presentan una disfunción cardiovascular in útero que persiste postnatalmente. Los resultados sugieren que el CIR induce cambios cardiacos primarios que podría explicar la mayor predisposición a patología cardiovascular en vida adulta.

APA, Harvard, Vancouver, ISO, and other styles

3

Tegethoff, Marion. "Fetal origins of pediatric disease fetoplacental plasticity and intrauterine programming by stress and glucocorticoids." Göttingen Cuvillier, 2009. http://d-nb.info/999629417/04.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Kelly, Amy, and Amy Kelly. "Adaptations in the Pancreatic Islet Transcriptome of Intrauterine Growth Restricted Fetuses." Diss., The University of Arizona, 2017. http://hdl.handle.net/10150/624586.

Full text

Abstract:

We established that acute adrenergic receptor stimulation in β-cells suppresses oxidative metabolism. This effect provides the basis for understanding how CAs reduce cell proliferation. Furthermore, the effects of acute CA on Min6 cells were distinguished from chronic CA culture using proteomics. Together, the RNAseq, qPCR and proteomic studies support a role for adrenergic receptor signaling in the regulation of proliferaton in β-cells. This work describes the genetic and proteomic profile underlying chronic adrenergic signaling and identifies CA independent suppression of β-cell growth and metabolism. Through the use of multiple models and comparative bioinformatics, we refined the list of molecular dysfunctions associated with the IUGR pathology to a set of specific and testable adrenergic targets.

APA, Harvard, Vancouver, ISO, and other styles

5

Huber, Hillary. "Aggressive Behavioral Phenotype in Intrauterine Growth Restricted (IUGR) Baboons Exposed to Moderate Nutrient Restriction Early in Development." OpenSIUC, 2014. https://opensiuc.lib.siu.edu/dissertations/824.

Full text

Abstract:

The thrifty phenotype hypothesis proposes reduced nutrition alters the trajectory of development of metabolic regulatory systems to produce a phenotype better fitted to an environment of decreased later-life nutrient availability. Because organisms have physiological mechanisms for coping with poor nutrition, they may have sociobehavioral mechanisms as well. Aggressive behavior, especially in the context of feeding competition, may be advantageous in such environments. There could be an association between aggression and intrauterine growth restriction (IUGR), which can result from low maternal food intake during pregnancy. The main hypotheses of this study are [1] IUGR offspring demonstrate higher rates of aggressive behavior and [2] IUGR offspring attain higher ranks. Behavioral observations were conducted on 22 juvenile baboons (Papio sp., ages 3-5 yrs) living in groups. Male IUGR (n = 4) and female IUGR (n = 5) were offspring of mothers fed 70% the same feed eaten by control (CTR) mothers in pregnancy and lactation. CTR males (n = 8) and CTR females (n = 5) were offspring of mothers fed ad libitum. Some authorities recommend this moderate level of dietary restriction for health and longevity. Offspring have not experienced dietary restriction since weaning. IUGR, compared to CTR, showed significantly increased rates of aggressive behavior, especially threat displays. Differences were more dramatic in males than in females. IUGR baboons performed the affiliative display behaviors lipsmack and chatter at elevated rates too, perhaps to counteract the effects of increased aggressive displays. IUGR females exhibited increased rates of stereotypical chewing behavior, while IUGR males exhibited decreased rates of play behavior, possibly indicating elevated anxiety levels. There was only limited support for condition-based differences in rank. Elevated rates of aggression in IUGR baboons may reflect an aggressive behavioral phenotype that enhances fitness by improving access to resources. Alternatively, they could be a non-adaptive result of neurodevelopment with a potentially negative impact on fitness. Unraveling the dynamic relationship between experiences and development is essential for understanding how phenotypes are formed. This will improve the ability of mothers to assess benefits of different nutritional strategies, leading to healthier individuals not just during growth and development, but throughout life.

APA, Harvard, Vancouver, ISO, and other styles

6

Alves, Márcio Bonesso. "Flexibilidade cognitiva em roedores adultos expostos à restrição de crescimento intrauterino : investigação do papel do cuidado materno e da resposta neuroquímica à recompensa." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2014. http://hdl.handle.net/10183/109720.

Full text

Abstract:

A restrição do crescimento intrauterino (RCIU) está associada com preferências alimentares alteradas, assim como com um aumento do risco de obesidade na vida adulta. Enquanto os desfechos metabólicos adversos têm sido de certa forma bem caracterizados nesta condição, seus déficits neurocomportamentais e alterações em áreas específicas do sistema nervoso têm recebido significativamente menos atenção. Além disso, o papel do cuidado materno no estabelecimento destes desfechos também deve ser avaliado. O objetivo deste estudo foi investigar os efeitos da RCIU sobre a flexibilidade cognitiva dos animais na vida adulta, explorando o possível envolvimento do cuidado materno e da resposta neuroquímica à recompensa – através da medida do conteúdo de tirosina hidroxilase (TH) no córtex orbitofrontal (OFC) e núcleo accumbens ( NAcc ) – sobre este desfecho. Materiais e Métodos: A partir do dia 10 de gestação e durante toda a lactação, ratas Sprague-Dawley receberam uma dieta ad libitum (Contr), ou uma dieta restrita a 50% do consumo médio das ratas do grupo Contr (FR). No dia do nascimento, foi realizada a adoção cruzada, gerando os grupos Contr/Contr e FR/Contr (gestação/lactação). Do dia 2 ao dia 7 pós-parto, o cuidado materno foi registrado em cinco sessões diárias de 72 minutos cada. A flexibilidade cognitiva foi medida nos ratos na idade adulta utilizando o Attentional Set- Shifting Task (ASST) que utiliza um pellet de alimento doce como recompensa. Os animais também foram submetidos a jejum de 4 horas e em seguida expostos ao alimento doce durante 1 hora para verificar o consumo agudo de alimento palatável. O conteúdo de TH no córtex orbitofrontal e núcleo accumbens foi medido em jejum ou em resposta à ingestão de alimentos palatáveis. Resultados: Ratas FR mostraram menos comportamentos de lamber os filhotes que fêmeas do grupo Contr (p<0,01) sem diferença nos escores das posturas de amamentação e no tempo permanecido em contato com os filhotes. Filhotes de ratas FR apresentaram peso reduzido ao nascer (p<0,01). Aos 90 dias de idade, machos do grupo FR/Contr apresentaram maior consumo de alimento doce no teste de exposição aguda (p=0,04), enquanto que as fêmeas não diferiram na quantidade consumida (p=0,37). Quando comparadas às controles, fêmeas RCIU necessitaram menos trials para alcançar o critério na etapa de Reversão 2 do ASST (p=0,04), e apresentaram um aumento de TH no OFC em resposta à ingestão de alimentos doces (p=0,04). Não foram observadas diferenças para o sexo masculino em relação à performance no ASST ou nos níveis de TH no OFC. No NAcc , houve um aumento de TH no estado de jejum tanto nos machos RCIU (p=0,03) quanto nas fêmeas RCIU (p=0,02). Discussão: O protocolo utilizado foi eficiente em induzir RCIU nos filhotes. Caracterizar os cuidado materno em diferentes protocolos é crucial para entender melhor as relações entre ambientes precoces adversos e seus coincidentes desfechos adversos na vida adulta. A melhora no desempenho do ASST e concomitante aumento de TH no OFC após consumo de doce sugere que as pistas relacionadas aos alimentos palatáveis sejam mais fortes para as fêmeas expostas à RCIU. Além disso, as alterações encontradas no Nacc em ambos os sexos sugere que a RCIU induz modificações na resposta central para as pistas de alimentos palatáveis e no consumo, afetando a liberação de dopamina em algumas estruturas do circuito encefálico de recompensa.
Intrauterine growth restriction (IUGR) is associated with altered food preferences as well as increased risk for obesity in adult life. However, while the adverse metabolic outcomes have been better characterized in this condition, the neurobehavioral disabilities and particular abnormalities in specific areas of the brain have received less attention. Moreover, the role of maternal care in the stablishment of these outcomes should be evaluated. The aim of this study was to investigate the effects of IUGR on the cognitive flexibility of adult animals, exploring the putative involvement of maternal care and the neurochemical response to reward – through the measurement of tyrosine hydroxylase (TH) content in the orbitofrontal (OF) cortex and nucleus accumbens (nacc) - on this behavioral outcome. Materials and methods: From day 10 of gestation and through lactation, Sprague-Dawley rats received either an ad libitum (AdLib), or a 50% food restricted (FR) diet. At birth, pups were cross-fostered, generating AdLib/AdLib and FR/AdLib groups (pregnancy/lactation). From day 2 to 7 postpartum maternal care was recorded in a five daily sessions. Cognitive flexibility was measured using the Attentional Set-Shifting Task (ASST) with a sweet pellet as a reward. Animals were also submitted to 4 hours of fasting and then exposed to a sweet food for 1 hour to verify the palatable food consumption. TH content in the OF cortex and Nacc was measured at baseline or in response to palatable food intake. Results: Dams of FR group showed less care toward her pups. More precisely, these FR dams showed less licking/grooming than AdLib dams (p<0.01), without difference in the nursing postures and time spent out of the nest. Pups of FR dams had reduced birth weight (p<0.01). At 90 days of age, FR/AdLib males showed increased intake of sweet food in the acute exposure (p=0.04), while females did not differ in the amount consumed (p=0.37). When compared to Controls, IUGR females needed fewer trials to reach criterion in the ASST(p=0.04) and had an increase in TH in response to sweet food intake in the OFC (p=0.04), but not at baseline. No differences were seen in males (p=0.51). In the nacc, there was an increase in TH at baseline in IUGR males (p=0.03) and females (p=0.02). Discussion: The protocol used was efficient in inducing IUGR in the pups. To characterize maternal care in different protocols is crucial to better understand the relationships between early adverse environment and their coincident adverse outcomes in adult life. The improvement in performance of FR females in ASST and concomitant increase in OFC TH in respone to sweet food consumption suggests that palatable food cues are stronger for intrauterine restricted females. Besides, alterations found in the Nacc in both sexes suggest that IUGR induces modifications in the central response to palatable food cues and its intake, affecting dopamine release in select structures of the brain reward system.

APA, Harvard, Vancouver, ISO, and other styles

7

Ekert, Jason Elliot. "Intrauterine programming of leptin / Jason Elliot Ekert." 2000. http://hdl.handle.net/2440/19853.

Full text

Abstract:

Includes bibliographical references.
xxiii, 1 v. (various pagings) : ill. (some col.) ; 30 cm.
Title page, contents and abstract only. The complete thesis in print form is available from the University Library.
The guinea pig and pig were evaluated as experimental animal models in which to investigate mechanisms of in utero leptin programming in humans.
Thesis (Ph.D.)--Adelaide University, Dept. of Obstetrics and Gynaecology, 2001

APA, Harvard, Vancouver, ISO, and other styles

8

Rueda-Clausen, Christian Federico. "Long-term cardiovascular and metabolic effects of hypoxia-induced intrauterine growth restriction." Phd thesis, 2011. http://hdl.handle.net/10048/1768.

Full text

Abstract:

Cardiovascular and metabolic diseases are still the primary cause of death and disability in modern society. Although genetic factors play a fundamental role in the development of these chronic conditions, the remarkable variability in an individual’s susceptibility to develop these pathologies cannot be completely explained by genetics. The early programming of adult diseases theory became established in the 1980’s, and is now supported by a growing body of evidence demonstrating that exposure to suboptimal environmental conditions during crucial periods of time can predispose an individual to the development of chronic conditions (including cardiovascular and metabolic diseases) later in life. Among the multitude of factors that can cause early programming, we have focused on the study of pregnancy complications leading to fetal hypoxia and causing intrauterine growth restriction (IUGR). To this end, we have used an animal model in which pregnant Sprague Dawley rats were exposed to either normal (∼21% O2) or hypoxic (∼11.5% O2) conditions during the last third of pregnancy. We then followed and studied the cardiovascular and metabolic characteristics of the offspring later in life. The studies presented in this thesis demonstrate that hypoxic prenatal insults have long-term consequences on cardiac structure, function and susceptibility to ischemia. We also demonstrated that programmed susceptibility to myocardial ischemia was associated with changes in cardiac energy metabolism and increased levels of myocardial oxidative stress. Moreover, we described the interaction between prenatal hypoxic insults, aging and sex differences in the later development of cardiovascular conditions. Additional studies presented in this thesis demonstrate that offspring born IUGR are more susceptible to develop most components of the metabolic syndrome when exposed to a high-fat (HF) diet. Furthermore, we also demonstrated that the exacerbated deleterious response to a HF diet described in offspring born IUGR can be prevented by postnatal administration of Resveratrol, which is a natural compound with anti-oxidant and anti-aging properties. In conclusion, the results presented in this thesis are an important contribution to the understanding of the long-term cardiovascular and metabolic effects of prenatal hypoxic insults causing IUGR and provide evidence regarding possible mechanisms and treatment alternatives that could be considered.

APA, Harvard, Vancouver, ISO, and other styles

9

Maftei, Oana. "Intrauterine influences on obesity and insulin resistance in pre-pubertal children." Thesis, 2012. http://hdl.handle.net/2440/75507.

Full text

Abstract:

Within the paradigm of developmental origins of health and disease, an intrauterine environment that stimulates fetal overnutrition has been found to contribute to the risk of subsequent obesity in the offspring. There is compelling epidemiological evidence for a positive association between maternal obesity prior to pregnancy, gestational diabetes (GD) or excessive gestational weight gain, and the development of childhood obesity (as measured by body mass index, BMI). However, the evidence is limited and inconsistent with respect to more specific measures of adiposity (body composition or fat pattern) and insulin resistance in children. Furthermore, the long-term effects of maternal borderline gestational glucose intolerance (BGGI) on the offspring have not been considered. Therefore, I sought to examine whether maternal obesity prior to pregnancy, gestational glucose intolerance across the entire spectrum, and gestational weight gain have deleterious effects on the development of obesity (both global and specific measures of adiposity) and insulin resistance in pre-pubertal children. These associations are particularly important from a public health perspective as, once identified, they may point towards potential windows for prevention of childhood obesity and related metabolic disorders. This project entailed a follow-up of an existing representative, prospective birth cohort study (Generation 1 Study, n=557) in Adelaide, South Australia, recruited during 1998-2000. At the 9-10 year follow-up, rigorous anthropometric measurements were conducted in 443 children (80% of the original cohort), of whom 163 consented to provide a fasting blood sample for the estimation of insulin resistance based on homeostasis model assessment (HOMA-IR). Information on intrauterine exposures and confounders was collected from the antenatal interviews and hospital records. Maternal age, parity, smoking, pregnancy-induced hypertension, and education at the time of pregnancy were considered as potential confounders for all the associations of interest, and child current BMI z-score as a potential mediator on the pathway between the intrauterine exposures and child insulin resistance. Data were analysed using multiple linear regression and generalized linear models. Maternal pre-pregnancy BMI was positively associated with all three obesity-related measures considered in the 9-10 year-old children (BMI z-score, percentage body fat estimated by bioelectrical impedance analysis, and waist-to-height ratio); these relationships were robust to adjustment for potential confounders (adjusted coefficients for each one kg/m2 increase in maternal pre-pregnancy BMI were 0.08 (95% confidence interval 0.06, 0.10) for child BMI z-score, 0.44 (95% CI 0.31, 0.58) for percentage body fat and 0.002 (95% CI 0.002, 0.003) for waist-to-height ratio). There was no association between maternal pre-pregnancy BMI and HOMA-IR in children (with or without adjustment); however, when child current BMI z-score was included as a mediating variable, the relationship between maternal pre-pregnancy BMI and child HOMA-IR was inverse and significant (adjusted change in child HOMA-IR for each one kg/m2 increase in maternal pre-pregnancy BMI was -0.83% (95% CI 1.63, -0.02)). Intrauterine exposure to glucose intolerance during pregnancy (either BGGI or GD) was not associated with any of the three obesity-related measures in children at 9-10 years. Children of mothers who developed GD during the index pregnancy had a higher HOMA-IR; this relationship was robust to adjustment for potential confounders (adjusted change in child HOMA-IR if exposed to maternal GD was 42.9% (95% CI 20.9, 68.9)) and partly mediated by child current BMI z-score. No association was found between exposure to maternal BGGI and child HOMA-IR (with or without confounder adjustment); however, when child current BMI z-score was added as a potential mediator, exposure to BGGI was associated with a reduction in child HOMA-IR (adjusted change in child HOMA-IR if exposed to maternal BGGI was -17.9% (95% CI -29.9, -3.96)). There were no significant associations between maternal gestational weight gain and any of the outcome measures of interest in unadjusted models. However, adjustment for pre-pregnancy BMI led to a positive association between gestational weight gain and child BMI z-score (adjusted changes in child BMI z-score for each one kg increase in maternal gestational weight gain was 0.032 (95% CI 0.007, 0.057)). Gestational weight gain was not associated with child insulin resistance, and this did not change when child current BMI z-score was included as a potential mediator on the pathway between gestational weight gain and child insulin resistance. Potential two-way interactions between the main exposures were investigated in relation to all outcomes of interest. Two significant interactions were identified: maternal pre-pregnancy BMI and glucose tolerance status, and maternal pre-pregnancy BMI and gestational weight gain, with a synergistic effect on child waist-to-height ratio. These results suggest that childhood obesity and insulin resistance have origins, at least in part, in intrauterine life, particularly in relation to maternal obesity at the time of pregnancy and GD. Further research to differentiate between genetic, environmental and intrauterine programming is recommended. That said, maternal pre-pregnancy BMI was the strongest predictor of child BMI zscore, while GD appeared to have an independent effect on child insulin resistance, and both clinical and public health actions to address these maternal factors are warranted for a range of reasons.
Thesis (Ph.D.) -- University of Adelaide, School of Population Health and Clinical Practice and School of Paediatrics and Reproductive Health, 2012

APA, Harvard, Vancouver, ISO, and other styles

Books on the topic "Intrauterine programming"

1

Seckl, Jonathan R., and Yves Christen, eds. Hormones, Intrauterine Health and Programming. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-02591-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Hormones, Intrauterine Health and Programming. Springer, 2014.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

3

Seckl, Jonathan R., and Yves Christen. Hormones, Intrauterine Health and Programming. Springer, 2014.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Intrauterine programming"

1

Cooper, Cyrus, Muhammad K. Javaid, Karen Walker-Bone, Elaine M. Dennison, and Nigel K. Arden. "The Intrauterine Programming of Osteoporosis." In Medical Science Symposia Series, 43–50. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1061-1_5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Jiao, Zhexiao, Hao Kou, Dan Xu, Hanwen Luo, and Hui Wang. "Intrauterine Programming and Effects of Caffeine." In Diet, Nutrition, and Fetal Programming, 339–53. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-60289-9_25.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Shin, Bo-Chul, and Sherin U. Devaskar. "Regulation of Skeletal Muscle GLUT4 in Intrauterine Growth Restriction Offspring." In Fetal and Early Postnatal Programming and Its Influence on Adult Health, 103–24. Boca Raton : Taylor & Francis, 2017. | Series: Oxidative stress and disease: CRC Press, 2017. http://dx.doi.org/10.1201/9781315154312-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Ortega-Márquez, Ana Laura, Angélica Morales-Miranda, and Sumiko Morimoto. "Impact of Epigenetic Mechanisms on the Regulation of Gene Expression During Intrauterine Programming of the Endocrine Pancreas." In Handbook of Nutrition, Diet, and Epigenetics, 777–92. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-55530-0_69.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Ortega-Márquez, Ana Laura, Angélica Morales-Miranda, and Sumiko Morimoto. "Impact of Epigenetic Mechanisms on the Regulation of Gene Expression During Intrauterine Programming of the Endocrine Pancreas." In Handbook of Nutrition, Diet, and Epigenetics, 1–16. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-31143-2_69-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Schäffer, Leonhard, Tilo Burkhardt, Maren Tomaske, Manfred Rauh, and Ernst Beinder. "6 Intrauterine corticosteroids for lung maturation: Observations of HPA axis function and cardiac autonomic balance in the neonate." In Perinatal Programming, edited by Andreas Plagemann. Berlin, Boston: DE GRUYTER, 2011. http://dx.doi.org/10.1515/9783110249453.51.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Glezerman, Marek. "Intrauterine Development of Sex Differences—Fetal Programming * *For easier reading, I will be using throughout this chapter the term “fetus” whenever I refer to the embryo or the fetus and I will use the term “mother” for the pregnant woman. Moreover, whenever I use throughout this chapter the terms “increased risk” for a certain type of pathology, I mean just that, namely that a preexisting risk may increase, but still leave the majority of children unaffected." In Principles of Gender-Specific Medicine, 237–49. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-803506-1.00039-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!