Placental structure and inflammation in pregnancies associated with obesity

Roberts, Kirsty; Riley, Simon C.; Reynolds, Rebecca M.; Barr, Sarah; Evans, M.; Statham, Aaron L.; Hor, Kahyee; Jabbour, Henry N.; Norman, Jane E.; Denison, Fiona C.

doi:10.1016/j.placenta.2010.12.023

Cited by 250 publications

(224 citation statements)

References 22 publications

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“…4 One antecedent that we identified, maternal obesity, is of particular interest because it is potentially modifiable and its prevalence is increasing. 48 Although maternal obesity is predictive of higher maternal blood levels of Creactive protein 49 and interleukin-6, 50 we found no indirect evidence to support a link between maternal inflammation, as indicated by placental findings and initiators of preterm delivery, and subsequent impaired infant cognitive function. Maternal obesity is associated with multiple complications of pregnancy 51 and with perinatal mortality.…”

Section: Discussioncontrasting

confidence: 66%

Antenatal Antecedents of Cognitive Impairment at 24 Months In Extremely Low Gestational Age Newborns

et al. 2012

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WHAT'S KNOWN ON THIS SUBJECT: Among extremely premature infants, survival has improved, but the rate of cognitive impairment has not. Impaired cognition is the most frequent developmental problem identified in survivors. Several antenatal factors have been associated with cognitive impairment, mostly related to social disadvantage. WHAT THIS STUDY ADDS:In addition to social disadvantage, antenatal characteristics associated with cognitive impairment include maternal obesity and thrombosis of fetal stem vessels. Prenatal infection and inflammation were not associated with impaired early cognitive function among extremely preterm infants. abstract BACKGROUND AND OBJECTIVES: Extremely low gestational age neonates are more likely than term infants to develop cognitive impairment. Few studies have addressed antenatal risk factors of this condition. We identified antenatal antecedents of cognitive impairment determined by the Mental Development Index (MDI) portion of the Bayley Scales of Infant Development, Second Edition (BSID-II), at 24 months corrected age. METHODS:We studied a multicenter cohort of 921 infants born before 28 weeks of gestation during 2002 to 2004 and assessed their placentas for histologic characteristics and microorganisms. The mother was interviewed and her medical record was reviewed. At 24 months adjusted age, children were assessed with BSID-II. Multinomial logistic models were used to estimate odds ratios. RESULTS:A total of 103 infants (11%) had an MDI ,55, and 99 infants (11%) had an MDI between 55 and 69. No associations were identified between organisms recovered from the placenta and developmental delay. Factors most strongly associated with MDI ,55 were thrombosis of fetal vessels (OR 3.1; 95% confidence interval [CI] 1.2, 7.7), maternal BMI .30 (OR 2.0; 95% CI 1.1, 3.5), maternal education #12 years (OR 3.4; 95% CI 1.9, 6.2), nonwhite race (OR 2.2; 95% CI 1.3, 3.8), birth weight z score , 22 (OR 2.8; 95% CI 1.1, 6.9), and male gender (OR 2.7; 95% CI 1.6, 4.5).CONCLUSIONS: Antenatal factors, including thrombosis of fetal vessels in the placenta, severe fetal growth restriction, and maternal obesity, convey information about the risk of cognitive impairment among extremely premature newborns. Pediatrics 2012;129:494-502

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Section: Discussioncontrasting

confidence: 66%

Antenatal Antecedents of Cognitive Impairment at 24 Months In Extremely Low Gestational Age Newborns

et al. 2012

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“…No placental maturity abnormalities, oedema, syncytial knots, fibrin deposition or chorangiosis have been shown. However, obese placentas displayed an increase in the muscularity of vessel walls in the villi (Roberts et al, 2011). In a non-human primate model where obesity was induced by a chronic high-fat diet, placentas showed an increase of infarction and chorionic villous calcification (Frias et al, 2011).…”

mentioning

confidence: 99%

Placental contribution to nutritional programming of health and diseases: epigenetics and sexual dimorphism

Tarrade

Panchenko

Junien

et al. 2015

Journal of Experimental Biology

204

149

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The recent and rapid worldwide increase in non-communicable diseases challenges the assumption that genetic factors are the primary contributors to such diseases. A new concept of the 'developmental origins of health and disease' (DOHaD) is at stake and therefore requires a paradigm shift. Maternal obesity and malnutrition predispose offspring to develop metabolic syndrome, a vicious cycle leading to transmission to subsequent generation(s), with differences in response and susceptibility according to the sex of the individual. The placenta is a programming agent of adult health and disease. Adaptations of placental phenotype in response to maternal diet and metabolic status alter fetal nutrient supply. This implies important epigenetic changes that are, however, still poorly documented in DOHaD studies, particularly concerning overnutrition. The aim of this review is to discuss the emerging knowledge on the relationships between the effect of maternal nutrition or metabolic status on placental function and the risk of diseases later in life, with a specific focus on epigenetic mechanisms and sexual dimorphism. Explaining the sex-specific causal variables and how males versus females respond and adapt to environmental perturbations should help physicians and patients to anticipate disease susceptibility.KEY WORDS: DOHaD, Fetal programming, Placenta, Sex, Nutrition, Obesity, Maternal environment, Gestation Introduction: developmental origins of health and diseaseThe recent and rapid worldwide increase in non-communicable diseases (NCDs) challenges the assumption that genetic factors are the primary contributors to such diseases (McAllister et al., 2009). The 'developmental origins of health and disease' (DOHaD) paradigm states that the environment during the periconception, gestation and lactation periods shapes the developing individuals, leading, in the case of a deleterious environment, to a predisposition to adult-onset diseases. This theory was popularised by D. J. Barker in the early 1990s (Barker, 1990) but the question had already been raised in earlier studies. In the 1960s and 1970s, different experiments on diverse mammalian species (rat, mouse, guinea pig, pig, etc.) showed that a reduction of maternal calorie or protein intake during pregnancy and lactation affects the growth capacity and cognitive ability of the offspring (reviewed in Roeder and Chow, 1972;McCance, 1976). Later, this concept was extended to phenotype in general, with a strong implication for quantitative traits in agriculture. An increasing number of studies pointed to the fact that maternal environment in cattle was an important parameter to fully express the genetically highly selected potential of the animals (Wallace et al., 2010; Jammes et al., 2011;Tanghe et al., 2014).Male and female susceptibility to NCDs is well described. It appears that in the DOHaD context, the same environmental exposure may affect the long-term health of the offspring with a discrepancy between males and females in terms of the timing, onset ...

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“…У беременных с диабетом, избыточной массой тела или ожирением цитокины выраба-тываются клетками иммунной системы, жировой тканью, а также плацентой [15,16,17], что может усугублять метаболические расстройства и прово-цировать развитие воспалительных реакций [1].…”

Section: Discussionunclassified

Cytokine Profile in Pregnant Women With Metabolic Disorders

Прохоренко¹,

Зима²,

Саприна³

et al. 2017

Med. immunol.

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Адрес для переписки:Прохоренко Татьяна Сергеевна ФГБОУ ВО «Сибирский государственный медицинский университет» Министерства здравоохранения РФ 634050, Россия, г. Томск, ул. Московский тракт, 2. Тел.: 8 (3822) 53-33-09. E-mail: mmikld.ssmu@gmail Медицинская иммунология, 2017. Т. 19, № 3. С. 301-306. doi: 10.15789/1563-0625-2017-3-301-306 © Прохоренко Т.С. и соавт., 2017 For citation: T.S. Prokhorenko, A.P. Zima, T.V. Saprina, V.V. Novitskiy, N.M. Todosenko, L.S. Litvinova "Cytokine profile in pregnant women with metabolic disorders", Medical Immunology (Russia)/ Meditsinskaya Immunologiya, 2017, Vol. 19, no. 3, pp. 301-306. doi: 10.15789/1563-0625-2017 Резюме. Методом проточной флюориметрии с использованием мультиплексной тест-системы проведено определение концентрации цитокинов (IL-2, IL-6, IL-8, IL-10, GM-CSF, IFNγ, TNFα) в сыворотке крови беременных в зависимости от вида метаболических нарушений: при гестационном сахарном диабете, ожирении и их сочетании. Изменение цитокинового профиля у беременных с из-быточной массой тела или ожирением и беременных с гестационныи сахарным диабетом оказалось значительно схожим. У беременных, имеющих избыточный вес или ожирение, выявлено повышение концентрации в крови IL-2, IL-6, IL-10, IFNγ и TNFα; у беременных с гестационным сахарным диа-бетом -повышение содержания в крови IL-2, IL-6, IL-10 и TNFα. При беременности, отягощенной гестационным сахарным диабетом и ожирением, изменения цитокинового профиля носили наибо-лее выраженный характер. У данных женщин определена повышенная концентрация в крови IL-6, TNFα, GM-CSF и IFNγ на фоне низкого содержания IL-2 и IL-10. Обсуждаются причины и послед-ствия развития у беременных субклинического воспаления. Дается заключение, что у беременных с метаболическими нарушениями субклиническое воспаление развивается с ранних стадий ожире-ния или нарушения углеводного обмена. Abstract. Serum concentrations of cytokines (IL-2, IL-6, IL-8, IL-10, GM-CSF, IFNγ, TNFα) were determined in blood serum of pregnant women with different types of metabolic disorders, i.e., gestational diabetes, obesity, and a combination of those disorders. The study was performed by means of flow fluorimetry, using a multiplex test system. Changes of cytokine profiles in pregnant women with overweight or obesity, and pregnant women with gestational diabetes showed some similarities. In pregnant women with overweight or

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Placental structure and inflammation in pregnancies associated with obesity

Cited by 250 publications

References 22 publications

Antenatal Antecedents of Cognitive Impairment at 24 Months In Extremely Low Gestational Age Newborns

Antenatal Antecedents of Cognitive Impairment at 24 Months In Extremely Low Gestational Age Newborns

Placental contribution to nutritional programming of health and diseases: epigenetics and sexual dimorphism

Cytokine Profile in Pregnant Women With Metabolic Disorders

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