Leptin and paraoxonase activity in cord blood from obese mothers

Ferretti, Gianna; Cester, Am M.; Bacchetti, Tiziana; Raffaelli, Francesca; Vignini, Arianna; Orici, Francesca; Martino, Cameron; Al, Tranquilli

doi:10.3109/14767058.2013.858319

Cited by 29 publications

(22 citation statements)

References 29 publications

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“…Leptin, a proinflammatory adipokine, not only is elevated in the maternal circulation of pregnant obese women but also is higher in the cord blood of their children than in children whose mothers are not obese. 32 Conversely, adiponectin, which has antiinflammatory properties and has shown inverse associations with asthma symptoms 33 and airway inflammation, 34 is decreased in obesity and is also decreased in newborns of obese mothers. 35 Alternatively, maternal obesity may influence the pathogenesis of asthma through exposure of the developing fetus to different dietary patterns.…”

Section: Discussionmentioning

confidence: 99%

Maternal Obesity in Pregnancy, Gestational Weight Gain, and Risk of Childhood Asthma

et al. 2014

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BACKGROUND AND OBJECTIVE: Environmental or lifestyle exposures in utero may influence the development of childhood asthma. In this meta-analysis, we aimed to assess whether maternal obesity in pregnancy (MOP) or increased maternal gestational weight gain (GWG) increased the risk of asthma in offspring. METHODS: We included all observational studies published until October 2013 in PubMed, Embase, CINAHL, Scopus, The Cochrane Database, and Ovid. Random effects models with inverse variance weights were used to calculate pooled risk estimates. RESULTS: Fourteen studies were included (N = 108 321 mother–child pairs). Twelve studies reported maternal obesity, and 5 reported GWG. Age of children was 14 months to 16 years. MOP was associated with higher odds of asthma or wheeze ever (OR = 1.31; 95% confidence interval [CI], 1.16–1.49) or current (OR = 1.21; 95% CI, 1.07–1.37); each 1-kg/m2 increase in maternal BMI was associated with a 2% to 3% increase in the odds of childhood asthma. High GWG was associated with higher odds of asthma or wheeze ever (OR = 1.16; 95% CI, 1.001–1.34). Maternal underweight and low GWG were not associated with childhood asthma or wheeze. Meta-regression showed a negative association of borderline significance for maternal asthma history (P = .07). The significant heterogeneity among existing studies indicates a need for standardized approaches to future studies on the topic. CONCLUSIONS: MOP and high GWG are associated with an elevated risk of childhood asthma; this finding may be particularly significant for mothers without asthma history. Prospective randomized trials of maternal weight management are needed.

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Section: Discussionmentioning

confidence: 99%

Maternal Obesity in Pregnancy, Gestational Weight Gain, and Risk of Childhood Asthma

et al. 2014

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“…Studies demonstrated that obesity and metabolic syndrome are characterized by chronic inflammation (Hotamisligil 2006). Pregnancy is a stage having increased susceptibility to oxidative stress (Casanueva and Viteri 2003; Patil et al 2007) and effects may be enhanced in obese mothers (Ferretti et al 2013; Rajasingam et al 2009; Sen et al 2014). Furthermore, studies have demonstrated that obese pregnant women may have enhanced systemic and placental inflammation (Stewart et al 2007) and increased pro-inflammatory cytokine expression in the placenta (Challier et al 2008), suggesting that maternal obesity and traffic air pollution exposure may act synergistically to impact fetal development.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, pregnancy is a state having enhanced susceptibility to oxidative stress (Casanueva and Viteri 2003; Patil et al 2007) which has implications for fetal growth (Weber et al 2014). These associations may be further modified by maternal obesity (Ferretti et al 2013; Rajasingam et al 2009; Sen et al 2014). …”

Section: Introductionmentioning

confidence: 99%

Associations between prenatal traffic-related air pollution exposure and birth weight: Modification by sex and maternal pre-pregnancy body mass index

Lakshmanan

Chiu

Coull

et al. 2015

Environmental Research

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Background Prenatal traffic-related air pollution exposure is linked to adverse birth outcomes. However, modifying effects of maternal body mass index (BMI) and infant sex remain virtually unexplored. Objectives We examined whether associations between prenatal air pollution and birth weight differed by sex and maternal BMI in 670 urban ethnically mixed mother-child pairs. Methods Black carbon (BC) levels were estimated using a validated spatio-temporal land-use regression (LUR) model; fine particulate matter (PM2.5) was estimated using a hybrid LUR model incorporating satellite-derived Aerosol Optical Depth measures. Using stratified multivariable-adjusted regression analyses, we examined whether associations between prenatal air pollution and calculated birth weight for gestational age (BWGA) z-scores varied by sex and maternal pre-pregnancy BMI. Results Median birth weight was 3.3±0.6 kg; 33% of mothers were obese (BMI ≥30 kg/m3). In stratified analyses, the association between higher PM2.5 and lower birth weight was significant in males of obese mothers (−0.42 unit of BWGA z-score change per IQR increase in PM2.5, 95%CI: −0.79 to −0.06) ( PM2.5 × sex × obesity Pinteraction=0.02). Results were similar for BC models (Pinteraction=0.002). Conclusions Associations of prenatal exposure to traffic-related air pollution and reduced birth weight were most evident in males born to obese mothers.

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“…Umbilical cord leptin levels are elevated in obese pregnancies (Ferretti et al, 2014;Karakosta et al, 2013;Walsh et al, 2014) and neonatal circulating leptin is elevated in offspring of obese mice (Samuelsson et al, 2008). Therefore, early life hyperleptinaemia may drive sympathetic hyperstimulation in the developing renal-cardiovascular system, leading to hypertension and cardiovascular dysfunction in adulthood (Briffa et al, 2014).…”

Section: Cardiovascular Systemmentioning

confidence: 99%

Developmental programming by maternal obesity in 2015: Outcomes, mechanisms, and potential interventions

Penfold

Ozanne

2015

Hormones and Behavior

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This article is part of a Special Issue "SBN 2014". Obesity in women of child-bearing age is a growing problem in developed and developing countries. Evidence from human studies indicates that maternal BMI correlates with offspring adiposity from an early age and predisposes to metabolic disease in later life. Thus the early life environment is an attractive target for intervention to improve public health. Animal models have been used to investigate the specific physiological outcomes and mechanisms of developmental programming that result from exposure to maternal obesity in utero. From this research, targeted intervention strategies can be designed. In this review we summarise recent progress in this field, with a focus on cardiometabolic disease and central control of appetite and behaviour. We highlight key factors that may mediate programming by maternal obesity, including leptin, insulin, and ghrelin. Finally, we explore potential lifestyle and pharmacological interventions in humans and the current state of evidence from animal models.

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Leptin and paraoxonase activity in cord blood from obese mothers

Abstract: Essential obesity in pregnancy is associated with hyperleptinemia. PON1 exerts an antioxidant role; therefore, our results demonstrated that obesity exposes to an increased susceptibility to oxidative damage in both mothers and newborns.

Cited by 29 publications

References 29 publications

Maternal Obesity in Pregnancy, Gestational Weight Gain, and Risk of Childhood Asthma

Maternal Obesity in Pregnancy, Gestational Weight Gain, and Risk of Childhood Asthma

Associations between prenatal traffic-related air pollution exposure and birth weight: Modification by sex and maternal pre-pregnancy body mass index

Developmental programming by maternal obesity in 2015: Outcomes, mechanisms, and potential interventions

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