placental insufficiency/дебелина

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Uteroplacental insufficiency increases visceral adiposity and visceral adipose PPARgamma2 expression in male rat offspring prior to the onset of obesity.

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Uteroplacental insufficiency (UPI) induced intrauterine growth restriction (IUGR) predisposes individuals to adult onset metabolic morbidities, including insulin resistance and cardiovascular disease. An underlying component of the development of these morbidities is adipose dysfunction;

Maternal Obesity and Male Genital Anomalies: Potential Role of Placental Insufficiency and Metabolic Syndrome.

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β2-Adrenergic receptor desensitization in perirenal adipose tissue in fetuses and lambs with placental insufficiency-induced intrauterine growth restriction.

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Placental insufficiency-induced intrauterine growth restriction (IUGR) fetuses have chronic hypoxaemia and elevated plasma catecholamine concentrations. In this study, we determined whether adrenergic responsiveness becomes desensitized in the perirenal adipose tissue of IUGR fetuses and lambs by

Preeclampsia, placental insufficiency, and autism spectrum disorder or developmental delay.

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OBJECTIVE Increasing evidence suggests that autism spectrum disorder (ASD) and many forms of developmental delay (DD) originate during fetal development. Preeclampsia may trigger aberrant neurodevelopment through placental, maternal, and fetal physiologic mechanisms. OBJECTIVE To determine whether

Catecholamines mediate multiple fetal adaptations during placental insufficiency that contribute to intrauterine growth restriction: lessons from hyperthermic sheep.

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Placental insufficiency (PI) prevents adequate delivery of nutrients to the developing fetus and creates a chronic state of hypoxemia and hypoglycemia. In response, the malnourished fetus develops a series of stress hormone-mediated metabolic adaptations to preserve glucose for vital tissues at the

Placental insufficiency contributes to fatty acid metabolism alterations in aged female mouse offspring.

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Intrauterine growth restriction (IUGR) is an accepted risk factor for metabolic disorders in later life, including obesity and type 2 diabetes. The level of metabolic dysregulation can vary between subjects and is dependent on the severity and the type of IUGR insult. Classical IUGR animal models

Fetal undernutrition, placental insufficiency and pancreatic β-cell development programming in utero.

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The prevalence of obesity and type 2 (T2D) diabetes is a major health concern in the United States and around the world. T2D is a complex disease characterized by pancreatic β-cell failure in association with obesity and insulin resistance in peripheral tissues. Although several genes associated

Impact of maternal obesity on fetal programming of cardiovascular disease.

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The in utero environment is a key determinant of long-term health outcomes; poor maternal metabolic state and placental insufficiency are strongly associated with these long-term health risks. Human epidemiological studies link maternal obesity and offspring cardiovascular disease in later life, but

Tacrolimus in the prevention of adverse pregnancy outcomes and diabetes-associated embryopathies in obese and diabetic mice.

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T2DM is a high-risk pregnancy with adverse fetal and maternal outcomes including repeated miscarriages and fetal malformations. Despite the established association between placental insufficiency and poor maternal Th1-adaptability to the development of pregnancy complications in T2DM, there have

Maternal diet-induced obesity and offspring cardiovascular health.

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It is widely recognized that environmental insults during adulthood including smoking, lack of exercise and a poor diet increases an individual's risk of cardiovascular disease (CVD). However, research initiated over the last two decades has highlighted that our risk of CVD can be programmed

Exposure to uteroplacental insufficiency reduces the expression of signal transducer and activator of transcription 3 and proopiomelanocortin in the hypothalamus of newborn rats.

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IUGR has been linked to the development of type 2 diabetes. Recent data suggest that some of the molecular defects underlying type 2 diabetes reside in the CNS. Disruption of the signal transducer and activator of transcription 3 (STAT3) in the hypothalamic neurons expressing leptin receptor,

The association of maternal obesity with fetal pH and base deficit at cesarean delivery.

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OBJECTIVE To evaluate the association between maternal body mass index (BMI) and umbilical cord acid-base status at the time of cesarean delivery. METHODS We conducted a retrospective multicenter cohort study using data from the Cesarean Section Registry of the Eunice Kennedy Shriver National

Neonatal management and long-term sequelae.

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Intrauterine or fetal growth restriction is best defined by using customised birth weight percentiles based upon the growth potential for an individual infant. Growth restriction in utero may be classified as asymmetric or symmetric depending upon the duration of the process. Asymmetric growth

A triple risk model for unexplained late stillbirth.

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BACKGROUND The triple risk model for sudden infant death syndrome (SIDS) has been useful in understanding its pathogenesis. Risk factors for late stillbirth are well established, especially relating to maternal and fetal wellbeing. CONCLUSIONS We propose a similar triple risk model for unexplained

Genetic selection of embryos that later develop the metabolic syndrome.

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THE BARKER HYPOTHESIS: Is an excellent explanation of the process where human and animal foetuses exposed to malnutrition, either by maternal malnutrition or placental insufficiency, are metabolically programmed, with selective stunting of cell differentiation and organ growth. With the postnatal

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