Intensive gestational glycemic management and childhood obesity: a systematic review and meta-analysis

Guillemette, Laetitia; Durksen, Anita; Rabbani, Rasheda; Zarychanski, Ryan; Abou‐Setta, Ahmed M; Duhamel, Todd A.; McGavock, Jonathan; Wicklow, Brandy

doi:10.1038/ijo.2017.65

Cited by 9 publications

(6 citation statements)

References 263 publications

(419 reference statements)

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“…Recently, Landon et al [44], in a follow-up study of 500 children, observed that GDM treatment improved neonatal health, but the frequency of obesity or metabolic dysfunction at ages 5-10 years was not reduced. A meta-analysis study corroborated these findings showing no association between intensive gestational glycemic management and reduction of childhood obesity in offspring [45]. We observed that although fasting glucose levels was above the ADA´s recommended levels [28], it was not sufficient to increase the percentage of Hb1Ac, demonstrating an efficient glycemic control.…”

Section: Discussionsupporting

confidence: 76%

BCL2 and miR-181a transcriptional alterations in umbilical-cord blood cells can be putative biomarkers for obesity

Marcondes

Andrade

Sávio

et al. 2018

Mutation Research/Genetic Toxicology and Environmental Mutagene

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Several findings suggest that in utero stressor stimuli can alter fetal development by promoting transcriptional changes, and predisposing the neonate to diseases later in life. This study aimed to investigate whether a hyperglycemic environment in pregnant women with gestational diabetes mellitus (GDM) is able to cause fetal genetic alterations and predispose neonates to obesity. Transcriptional alteration of SIRT1, TP53 and BCL2 genes, miR-181a (a SIRT1 or BCL2 regulator) and telomere length were evaluated in placental and umbilical-cord blood cells. Healthy (HP; n = 20) and GDM (n = 20) pregnant women and their respective neonates were included in the study. Additionally, obese (n = 20) and eutrophic (n = 20) adults also participated as reference populations. Gene expression data showed down-regulation of BCL2 in umbilical-cord and peripheral blood cells from GDM neonates and obese adults, respectively. The miR-181a was down-regulated only in umbilical-cord blood cells of GDM neonates. Telomere length presented no significant difference. In conclusion, our study demonstrated that the GDM hyperglycemic intrauterine environment promotes transcriptional alterations in BCL2 and miR-181a in neonate umbilical-cord blood cells. Furthermore, both GDM neonates and obese subjects share the same transcriptional alteration in BCL2. Considering the relationship between obesity development and the functions regulated by these two genes, BCL2 and miR-181a could be adopted as potential biomarkers for childhood obesity. However, further study designs are recommended to confirm this hypothesis.

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Section: Discussionsupporting

confidence: 76%

BCL2 and miR-181a transcriptional alterations in umbilical-cord blood cells can be putative biomarkers for obesity

Marcondes

Andrade

Sávio

et al. 2018

Mutation Research/Genetic Toxicology and Environmental Mutagene

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“…The findings that newborn adiposity and cord C-peptide mediate a significant proportion of the association between maternal glycemia and childhood adiposity support the use of these newborn measures as shorter-term outcome measures when investigating treatment strategies for gestational diabetes mellitus, with the ultimate goal of reducing childhood adiposity. A number of interventional studies in women with gestational diabetes mellitus have reported reductions in birth weight after treatment (30)(31)(32), while one reported reduced neonatal adiposity among treated mothers (33). However, the effect of maternal treatment on childhood adiposity is not clear.…”

Section: Discussionmentioning

confidence: 99%

Newborn Adiposity and Cord Blood C-Peptide as Mediators of the Maternal Metabolic Environment and Childhood Adiposity

et al. 2021

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OBJECTIVE Excessive childhood adiposity is a risk factor for adverse metabolic health. The objective was to investigate associations of newborn body composition and cord C-peptide with childhood anthropometrics and explore whether these newborn measures mediate associations of maternal midpregnancy glucose and BMI with childhood adiposity. RESEARCH DESIGN AND METHODS Data on mother/offspring pairs (N = 4,832) from the epidemiological Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study and HAPO Follow-up Study (HAPO FUS) were analyzed. Linear regression was used to study associations between newborn and childhood anthropometrics. Structural equation modeling was used to explore newborn anthropometric measures as potential mediators of the associations of maternal BMI and glucose during pregnancy with childhood anthropometric outcomes. RESULTS In models including maternal glucose and BMI adjustments, newborn adiposity as measured by the sum of skinfolds was associated with child outcomes (adjusted mean difference, 95% CI, P value) BMI (0.26, 0.12–0.39, <0.001), BMI z-score (0.072, 0.033–0.11, <0.001), fat mass (kg) (0.51, 0.26–0.76, <0.001), percentage of body fat (0.61, 0.27–0.95, <0.001), and sum of skinfolds (mm) (1.14, 0.43–1.86, 0.0017). Structural equation models demonstrated significant mediation by newborn sum of skinfolds and cord C-peptide of maternal BMI effects on childhood BMI (proportion of total effect 2.5% and 1%, respectively), fat mass (3.1%, 1.2%), percentage of body fat (3.6%, 1.8%), and sum of skinfolds (2.9%, 1.8%), and significant mediation by newborn sum of skinfolds and cord C-peptide of maternal glucose effects on child fat mass (proportion of total association 22.0% and 21.0%, respectively), percentage of body fat (15.0%, 18.0%), and sum of skinfolds (15.0%, 20.0%). CONCLUSIONS Newborn adiposity is independently associated with childhood adiposity and, along with fetal hyperinsulinemia, mediates, in part, associations of maternal glucose and BMI with childhood adiposity.

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“…In an Australian trial, more intensive treatment of gestational diabetes reduced macrosomia and pregnancy complications but there was no reduction in BMI in the children at 4-5 years of age66. Two other small trials, with follow-up of the children up to 10 years of age, have shown similar findings67. There is a need for large well-designed RCTs to assess the benefits of interventions to prevent or treat gestational diabetes and the cardio-metabolic health of the offspring.…”

Section: Effect Of Interventions In Early Life On Cardio-metabolic Oumentioning

confidence: 90%

Metabolic programming in early life in humans

Fall

Kumaran

2019

Phil. Trans. R. Soc. B

101

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Summary An association of low birth weight with an increased risk of adult cardiovascular disease and diabetes led to the developmental origins of health and disease (DOHaD) hypothesis, which proposes that undernutrition during early development permanently ‘programmes’ organ structure and metabolism, leading to vulnerability to later cardio-metabolic disease. High birth weight caused by maternal gestational diabetes is also associated with later diabetes, suggesting that fetal over-nutrition also has programming effects. Post-natal factors (excess weight gain/obesity, smoking, poor diets and physical inactivity) interact with fetal exposures to increase disease risk. Animal studies have shown permanent metabolic effects in offspring after alterations to maternal or early post-natal diets but evidence in humans is largely limited to observational and quasi-experimental situations such as maternal famine exposure. Randomised trials of maternal nutritional interventions during pregnancy have limited follow-up so far of the offspring. Moreover interventions usually started after the first trimester and therefore missed key peri-conceptional or early pregnancy events such as epigenetic changes, placentation and fetal organogenesis. Recent and ongoing trials, intervening pre-conceptionally and powered for long-term offspring follow-up will address these issues. While current preventive strategies for cardio-metabolic disease focus on high risk individuals in mid-life, DOHaD concepts offer a ‘primordial’ preventive strategy to reduce disease in future generations by improving fetal and infant development.

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Intensive gestational glycemic management and childhood obesity: a systematic review and meta-analysis

Cited by 9 publications

References 263 publications

BCL2 and miR-181a transcriptional alterations in umbilical-cord blood cells can be putative biomarkers for obesity

BCL2 and miR-181a transcriptional alterations in umbilical-cord blood cells can be putative biomarkers for obesity

Newborn Adiposity and Cord Blood C-Peptide as Mediators of the Maternal Metabolic Environment and Childhood Adiposity

Metabolic programming in early life in humans

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