Maternal obesity associated with inflammation in their children

Leibowitz, Karen L.; Moore, Reneé H.; Ahima, Rexford S.; Stunkard, Albert J.; Stallings, Virginia A.; Berkowitz, Robert I.; Chittams, Jesse; Faith, Myles S.; Stettler, Nicolas

doi:10.1007/s12519-011-0292-6

Cited by 52 publications

(52 citation statements)

References 19 publications

(29 reference statements)

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“…Likewise, maternal obesity in sheep and non-human primates has been shown to induce inflammation in the placenta, fetal liver, heart and intestine (26–28). The placenta in obese women is likewise characterized by inflammation and associated with increased systemic LPS levels (29–32). Our previous studies demonstrated activation of JNK and NF-κB pathways in placenta from obese women (33).…”

Section: Discussionmentioning

confidence: 99%

Maternal pregravid obesity changes gene expression profiles toward greater inflammation and reduced insulin sensitivity in umbilical cord

et al. 2014

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BackgroundMaternal obesity is associated with unfavorable outcomes, which may be reflected in the as yet undiscovered gene expression profiles of the umbilical cord (UC).MethodsUCs from 12 lean (pre-gravid BMI < 24.9) and 10 overweight/obese (OW/OB, pre-gravid BMI ≥25) women without gestational diabetes were collected for gene expression analysis using Human Primeview microarrays (Affymetrix). Metabolic parameters were assayed in mother’s plasma and cord blood.ResultsAlthough offspring birth weight and adiposity (at 2-wk) did not differ between groups, expression of 232 transcripts was affected in UC from OW/OB compared to those of lean mothers. GSEA analysis revealed an up-regulation of genes related to metabolism, stimulus and defense response and inhibitory to insulin signaling in the OW/OB group. We confirmed that EGR1, periostin, and FOSB mRNA expression was induced in UCs from OW/OB moms, while endothelin receptor B, KFL10, PEG3 and EGLN3 expression was decreased. Messenger RNA expression of EGR1, FOSB, MEST and SOCS1 were positively correlated (p<0.05) with mother’s first trimester body fat mass (%).ConclusionsOur data suggest a positive association between maternal obesity and changes in UC gene expression profiles favoring inflammation and insulin resistance, potentially predisposing infants to develop metabolic dysfunction later on in life.

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Section: Discussionmentioning

confidence: 99%

Maternal pregravid obesity changes gene expression profiles toward greater inflammation and reduced insulin sensitivity in umbilical cord

et al. 2014

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“…41 Furthermore, there is evidence that prepubescent children of women who were obese during pregnancy were dramatically more likely to have detectable C-reactive protein levels than children of non-obese mothers, even after controlling for the child's BMI and other potential confounding factors. 42 There is convincing evidence that intrauterine inflammation and fetal systemic inflammation are associated with an increased risk of brain injury leading to neurodevelopmental disability, such as cerebral palsy. 43,44 It is possible that the potential effects of increased inflammation in obese women, even in the absence of clinical signs or symptoms, is sufficient to significantly alter brain development in some children.…”

Section: Discussionmentioning

confidence: 99%

“…1 Limitation in intellectual ability corresponds to an intelligence quotient (IQ) of <70, described as mild (IQ 55-70), moderate (IQ [40][41][42][43][44][45][46][47][48][49][50][51][52][53][54][55], or severe to profound (IQ of <40). 2 The prevalence of ID in the general population is estimated to be approximately 1%, and among those with ID 85% are characterised as having mild ID.…”

Section: Introductionmentioning

confidence: 99%

Pre‐pregnancy body mass index, weight change during pregnancy, and risk of intellectual disability in children

Mann

McDermott

Hardin

et al. 2012

BJOG

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Objective This study investigated pre-pregnancy body mass index (BMI) and weight change in pregnancy as potential risk factors for intellectual disability (ID) in children.Design Retrospective cohort study.Setting South Carolina, USA. Methods We analysed South Carolina Medicaid data, linked to data from both the South Carolina Department of Education (DOE) and the South Carolina Department of Disabilities and Special Needs (DDSN). Maternal pre-pregnancy BMI and weight change during pregnancy were obtained from birth certificates. ID cases were identified from the three sources listed above. We used generalised estimating equation logistic regression models to model the odds of ID in children.Main outcome measures Identified as having ID in special education, DDSN, or Medicaid billing records.Results The risk of ID was greater in children of women with prepregnancy obesity, and the risk was greatest in children born to women with morbid obesity (OR 1.52, 95% CI 1.30-1.77 for ID of any severity; OR 1.73, 95% CI 1.23-2.45 for severe ID). Gestational weight change (gain or loss) was not significantly associated with odds of ID.Conclusions Pre-pregnancy obesity may be a modifiable risk factor for ID in children, although further study is needed to evaluate whether the association meets criteria for causation.

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“…An increasing number of publications indicate that maternal obesity can result in chronic inflammation and oxidative stress [7]. These conditions may, for example, impair placentation and establishment of adequate blood supply, perhaps altering fetal metabolism [8].…”

Section: How Do Maternal Obesity and Diet Influence The Early Nutritimentioning

confidence: 99%

Early Life Nutritional Programming of Obesity: Mother-Child Cohort Studies

et al. 2013

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Background: The obesity epidemic has resulted in more overweight/obese women before and during pregnancy. Their offspring tend to have higher birth weights and more body fat, and carry an increased risk of obesity later in life. These effects may partly be related to the heightened risk of gestational diabetes, occurring in at least 16% of all pregnancies irrespective of current body weight. Methods: An ILSI Europe workshop reviewed the key contributors leading to adverse outcomes in pregnancy and childhood, including gestational weight gain and nutrition. New research opportunities from prospective mother-child cohort studies were explored. Results: Simple measures of gestational weight gain provide insufficient detail of the underlying physiological and metabolic adaptations occurring in pregnancy, and should be complemented by measures of body composition, metabolic and endocrine responses. Recordings of maternal dietary intake and nutrient status are often limited and potential correlations with gestational weight gain have been poorly studied. Many pregnancies in overweight/obese women are uncomplicated and result in offspring of normal weight, leaving the main determinants of later adverse outcomes to be clarified. Conclusions: The workshop provided insights of primary measurements for the characterization of sustainable nutritional intervention strategies in the mother, infant and child for preventing obesity in later life.

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Maternal obesity associated with inflammation in their children

Abstract: These results suggest that maternal obesity during pregnancy is associated with later development of elevated hs-CRP in the offspring, even after controlling for weight.

Cited by 52 publications

References 19 publications

Maternal pregravid obesity changes gene expression profiles toward greater inflammation and reduced insulin sensitivity in umbilical cord

Maternal pregravid obesity changes gene expression profiles toward greater inflammation and reduced insulin sensitivity in umbilical cord

Pre‐pregnancy body mass index, weight change during pregnancy, and risk of intellectual disability in children

Early Life Nutritional Programming of Obesity: Mother-Child Cohort Studies

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