Gestational diabetes and childhood obesity

aDivision of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention bUS Public Health Service Commission Corps, Atlanta, Georgia, USA.
Current opinion in obstetrics & gynecology (Impact Factor: 2.07). 12/2012; 24(6):376-81. DOI: 10.1097/GCO.0b013e328359f0f4


Purpose of review:
To review recently published studies examining the role of prepregnancy obesity in the relationship between gestational diabetes mellitus and childhood obesity.

Recent findings:
Seven epidemiologic studies published from January 2011 to February 2012 differentiate between preexisting diabetes mellitus and gestational diabetes mellitus, and six of them examine the role of maternal obesity. In studies that account for maternal obesity as a covariate, the association between gestational diabetes mellitus and childhood obesity is attenuated significantly after adjustment for prepregnancy BMI. In the one study that does not adjust for maternal obesity, maternal glucose level during pregnancy is associated with greater offspring adiposity, independent of the child's diet and lifestyle.

This review shows a positive association between maternal gestational diabetes mellitus and offspring overweight and obesity that is attenuated significantly after adjustment for prepregnancy BMI. The relationship between maternal gestational diabetes mellitus and offspring overweight and obesity could reflect fetal programming, shared genes and/or shared environments, such as postnatal diet and physical activity. Maternal gestational hyperglycemia and subsequent fetal hyperinsulinemia may predispose offspring to increased adiposity, impaired glucose tolerance, hyperinsulinemia, and insulin resistance. Because maternal obesity is a more prevalent condition than gestational diabetes mellitus and strongly associated with offspring obesity, effective interventions addressing prepregnancy obesity need to be further explored as they may have a greater public health impact on childhood overweight and obesity than those targeting women with gestational diabetes mellitus.

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    • "Obesity and diabetes are more common in childhood and adolescence when there is a history of maternal or gestational diabetes. Under these conditions, metabolic disorders can affect the growth and the metabolism of the offspring and their subsequent generations [14]. There are many drugs to control glycemia, but they are usually expensive and are linked to concerns of congenital anomalies. "
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    ABSTRACT: Aim Investigate if the maternal use of flaxseed oil prevents pancreatic alterations in the offspring of diabetic mothers. Methods Diabetes was induced in female wistar rats (n = 12) by a high-fat diet and low-dose of streptozotocin. After the confirmation of the diabetes (glucose > 300 mg/dL), rats were mated and once pregnancy was confirmed, they were allocated into three groups (n = 6): High-Fat Group (HFG); Flaxseed Oil Group (FOG); and, Control Group (CG) (nondiabetic rats). At weaning, male offspring (n = 12/group) received a standard chow diet. The animals were euthanized in two phases: at 100 and at 180 days, (n = 6/group). The pancreas was collected for histomorphometric and immunohistochemistry analysis. Results HFG showed hypertrophy of pancreatic islets at 100 and at 180 days (p < 0.0001), while the FOG offspring had islets with smaller diameters compared to HFG at both phases of sacrifice (p < 0.0001). HFG had a lower percentage of small islets when compared to CG and FOG, which had a higher percentage when compared to HFG (p = 0.0053) at 100 days. At 180 days HFG showed higher percentage of larger islets (p = 0.00137) and lower percentage of smaller islets (p = 0.00112), when compared to FOG. HFG showed lower islet insulin imunnodensity at 100 days (p < 0.0001) and 180 days (p < 0.0001), whereas FOG was similar to CG (p < 0.0001) at 100 days and higher at 180 days (p < 0.0001). Conclusions Flaxseed oil reduced the damage caused by maternal hyperglycemia, promoting normal pancreas histomorphometry and β cell mass.
    Diabetes Research and Clinical Practice 10/2014; 106(3). DOI:10.1016/j.diabres.2014.09.022 · 2.54 Impact Factor
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    • "increased risk of T2D and cardiovascular disease, is most apparent when accompanied by maternal diabetes, both gestational and pregestational [8] [9]. Maternal pregestational obesity, with or without excessive weight gain during pregnancy, provides an equivalent risk for maternal hyperglycemia and infant macrosomia as does diabetes, and the offspring in both conditions exhibit a greater risk of obesity during adolescence [10] [11]. "
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    ABSTRACT: Objective. To examine the relationships between birth weight and body mass index, percent body fat, blood lipids, glycemia, insulin resistance, adipokines, blood pressure, and endothelial function in a cohort of obese adolescents. Design and Methods. Ninety-five subjects aged 10-16 years (mean age 13.5 years) with a body mass index >95th centile (mean [±SEM] 33.0 ± 0.6) were utilized from two prospective studies for obesity prevention prior to any interventions. The mean term birth weight was 3527 ± 64 g (range 1899-4990 g;). Results. Body mass index z-score correlated positively with birth weight (r (2) = 0.05, P = 0.03), but not percent body fat. Insulin resistance negatively correlated with birth weight (r (2) = 0.05, P < 0.001), as did fasting plasma insulin (r (2) = 0.05, P < 0.001); both being significantly greater for subjects of small versus large birth weight (Δ Homeostasis Model Assessment = 2.5 and Δ insulin = 10 pmol/L for birth weight <2.5 kg versus >4.5 kg). Adiponectin, but not leptin, blood pressure z-scores or peripheral arterial tomography values positively correlated with birth weight (r (2) = 0.07, P = 0.008). Conclusions. Excess body mass index in obese adolescents was positively related to birth weight. Birth weight was not associated with cardiovascular risk factors but represented a significant determinant of insulin resistance.
    08/2013; 2013:490923. DOI:10.1155/2013/490923
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    • "The resulting abnormal placenta environment may have deleterious effects on fetal metabolic programming and lead to the increased adverse perinatal outcomes , not only perinatal mortality, macrosomia , shoulder dystocia [3], but also preeclampsia [4] [5]. GDM and obesity in pregnancy often increase the risk for the baby to develop metabolic syndrome later in life [4] [6]. "
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    ABSTRACT: Metabolic impairments in maternal obesity and gestational diabetes mellitus (GDM) induce an abnormal environment in peripheral blood and cause vascular structure alterations which affect the placental development and function. A GDM model was developed using C57BL/6J female mice fed with high fat food (HF) (40% energy from fat) and a control group with control food (CF) (14% energy from fat) for 14 weeks before mating and throughout the gestation period. A subset of dams was sacrificed at gestational day (GD) 18.5 to evaluate the fetal and placental development. HF-fed dams exhibited significant increase in the maternal weight gain and homeostasis model assessment for insulin resistance index (HOMA-IR), impaired insulin secretion of glucose stimulus and glucose clearance of insulin stimulus before pregnancy; in addition, they also had the increase in the fetal and placental weight. HF-fed dams at GD 18.5 showed the high level of circulating maternal inflammation factors and were associated with increased oxidative stress and hypoxia in the labyrinth, abnormal vascular development with a high level of hypoxia inducible factor-1α (HIF-1α) and VEGF-A expression, but without a parallel increase in CD31 level; were induced an exaggerated inflammatory response in placental vascular endothelial cell. Our findings show that GDM induces more maternal weight gain and fetus weight, with abnormal maternal circulating metabolic and inflammation factors, and forms a placental hypoxia environment and impacts the placental vascular development. Our findings indicate that gestational diabetes induce excessive chronic hypoxia stress and inflammatory response in placentas which may contribute mechanisms to the high risks of perinatal complications of obesity and GDM mothers.
    International journal of clinical and experimental pathology 04/2013; 6(4):650-9. · 1.89 Impact Factor
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