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Childhood overweight and obesity prevalences (%) across the first decade of life among 13,037 normal birth weight children, stratified by maternal glucose (a) and gestational weight gain (b). Childhood overweight (>85 %ile) is indicated by dashed lines, and childhood obesity (>95 %ile) is indicated by solid lines. Childhood overweight and obesity were evaluated as repeated measures analysis (measures in multiple age-periods per child). Maternal glucose from gestational diabetes (GDM) screening was defined as: (1) Normal GCT [referent group]; (2) +GCT, No GDM [zero or one abnormality on OGTT; two or more abnormalities are required to diagnose GDM]; (3) GDM by C&C criteria. [2] GDM, mild hyperglycemia not diagnostic for GDM, and excessive maternal weight gain all significantly increased the risk of developing childhood overweight (>85 %ile) and obesity (>95 %ile) across the first decade of life (p < 0.0001 for all trends and all within group comparisons, after adjustment for maternal age, parity, baby gender, nonwhite race, child-birth year, as well as excessive maternal weight gain (a), and maternal GDM status (b)]

Childhood overweight and obesity prevalences (%) across the first decade of life among 13,037 normal birth weight children, stratified by maternal glucose (a) and gestational weight gain (b). Childhood overweight (>85 %ile) is indicated by dashed lines, and childhood obesity (>95 %ile) is indicated by solid lines. Childhood overweight and obesity were evaluated as repeated measures analysis (measures in multiple age-periods per child). Maternal glucose from gestational diabetes (GDM) screening was defined as: (1) Normal GCT [referent group]; (2) +GCT, No GDM [zero or one abnormality on OGTT; two or more abnormalities are required to diagnose GDM]; (3) GDM by C&C criteria. [2] GDM, mild hyperglycemia not diagnostic for GDM, and excessive maternal weight gain all significantly increased the risk of developing childhood overweight (>85 %ile) and obesity (>95 %ile) across the first decade of life (p < 0.0001 for all trends and all within group comparisons, after adjustment for maternal age, parity, baby gender, nonwhite race, child-birth year, as well as excessive maternal weight gain (a), and maternal GDM status (b)]

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Objective To determine, among children with normal birth weight, if maternal hyperglycemia and weight gain independently increase childhood obesity risk in a very large diverse population. Methods Study population was 24,141 individuals (mothers and their normal birth weight offspring, born 1995–2003) among a diverse population with universal GDM s...

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... Exposure to maternal obesity in utero is associated with obesity and metabolic disease later in life [1][2][3][4][5][6][7][8][9]. While the underlying biological mechanisms of these associations are not fully understood, it is posited that factors in the intrauterine environment have a direct effect on the metabolic function of fetal tissues. ...
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Background: Exposure to intrauterine obesity can disrupt clock gene rhythmicity in animal models. The aim of this pilot study was to determine if maternal obesity alters rhythmic expression of core clock in mesenchymal stem cells (MSCs) from umbilical cords of human infants born to mothers with obesity (Ob-MSC) vs. normal weight (NW-MSC). Methods: We compared in vitro rhythmic expression patterns of core clock (BMAL1, CLOCK, PER2) and clock-output (NR1D1), components in undifferentiated Ob-MSCs (n = 3) vs. NW-MSCs (n = 3). MSCs were harvested every 2 h, following a dexamethasone shock, for 30 h. Adipogenesis or myogenesis was induced in vitro and markers of adipogenesis and fat storage were assessed, respectively. Results: We detected significant rhythmicity in expression patterns of BMAL1, PER2, and NR1D1 at the group level in Ob- and NW-MSCs (p < 0.05). PER2 oscillatory amplitude was 3-fold higher in Ob-MSCs vs. NW-MSCs (p < 0.006). During adipogenesis, Ob-MSCs had higher PPARγ protein content (p = 0.04) vs. NW-MSC. During myogenesis, Ob-MSCs had higher saturated triacylglycerols (p = 0.04) vs. NW-MSC. Conclusion: Rhythmic expressions of BMAL1, PER2, and NR1D1 are detectable in undifferentiated MSCs. Higher PER2 oscillatory amplitude was paralleled by higher markers of fat storage during differentiation in Ob-MSCs vs. NW-MSCs, and supports that the core clock and cellular metabolism may be linked in infant MSCs.
... Obesity risk has been shown to increase sequentially with age, more so during mid-childhood (Gao et al., 2022). In two large cohort studies, GDM was associated with childhood obesity roughly within the first decade of life (Hillier et al., 2016;Lowe et al., 2018). However, in this study, excess maternal GWG and fetal exposure to GDM did not significantly influence the risk for childhood obesity by age 6 years. ...
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Introduction Excessive maternal gestational weight gain (GWG) is strongly correlated with childhood obesity, yet how excess maternal weight gain and gestational diabetes mellitus (GDM) interact to affect early childhood obesity is poorly understood. The purpose of this study was to investigate whether overall and trimester-specific maternal GWG and GDM were associated with obesity in offspring by age 6 years. Methods A cohort of 10,335 maternal-child dyads was established from electronic health records. Maternal weights at conception and delivery were estimated from weight trajectory fits using functional principal components analysis. Kaplan–Meier curves and Cox regression, together with generalized raking, examined time-to-childhood-obesity. Results Obesity diagnosed prior to age 6 years was estimated at 19.7% (95% CI: 18.3, 21.1). Maternal weight gain during pregnancy was a strong predictor of early childhood obesity (p < 0.0001). The occurrence of early childhood obesity was lower among mothers with GDM compared with those without diabetes (adjusted hazard ratio = 0.58, p = 0.014). There was no interaction between maternal weight gain and GDM (p = 0.55). Higher weight gain during the first trimester was associated with lower risk of early childhood obesity (p = 0.0002) whereas higher weight gain during the second and third trimesters was associated with higher risk (p < 0.0001). Discussion Results indicated total and trimester-specific maternal weight gain was a strong predictor of early childhood obesity, though obesity risk by age 6 was lower for children of mothers with GDM. Additional research is needed to elucidate underlying mechanisms directly related to trimester-specific weight gain and GDM that impede or protect against obesity prevalence during early childhood.
... Однако полученные результаты не всегда однозначны и в большинстве случаев противоречивы. По данным одних авторов, была установлена ассоциация ГСД, увеличения массы тела и частоты ожирения у детей в течение первых 10 лет жизни [15], в то время как в другом исследовании данных ассоциаций не прослеживалось [16]. Проведенная нами работа позволила оценить и сравнить антропометрические показатели детей до возраста 2 лет. ...
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... Inadequate GWG is associated with an increased risk of preterm delivery, 2 smallfor-gestational-age and low birthweight infants. 2 3 Excessive GWG is associated with increased risks of caesarean delivery, 3 pregnancy-related hypertension, 4 diabetes, 5 large-for-gestational-age infants and overweight and obese children. 6 Excessive GWG is also associated with an increased risk of postpartum weight retention 3 and subsequent maternal obesity. ...
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Obesity is an important health problem in many countries. Obesity among the child population is growing steadily, including the Russian Federation. Development of this disease often occurs in childhood and sometimes the origin of obesity goes back to prenatal period. There are a number of endogenous and exogenous factors than play an important role in development of obesity. These are heredity, socioeconomic status of the family, factors which are revealed during pregnancy and child delivery — weight gain, administration of antibacterial drugs and hyperglycemia in mother during her pregnancy, mode of delivery, feeding type and time of complementary food introduction, excessive consumption of calories with food, improper daily routine and lack of sleep, skipping meals, use of gadgets and associated physical inactivity and excessive food intake, marketing of high-calorie foods and others. Prevailing risk factors can be identified for each age period. Study and early identification of risk factors taking into account age of a child is necessary to take timely prevention measures and inform parents and their children about possible reasons and consequences of obesity.
... Childhood obesity is a global public health crisis in need of efficacious prevention strategies (1). Several observational studies in humans show that exposure to maternal obesity in utero is associated with obesity and metabolic disease risk later in life (2)(3)(4)(5)(6)(7)(8)(9)(10). This is in alignment with the Developmental Origins of Health and Disease (DOHaD) hypothesis, which posits that the propensity for obesity may be affected during fetal development. ...
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Exposure to maternal obesity may promote metabolic dysfunction in offspring. We use infant mesenchymal stem cells (MSC) to experimentally examine cellular mechanisms of intergenerational health transmission. Our earlier reports show MSCs collected from infants of mothers with obesity had a dichotomous distribution in metabolic efficiency; they were either efficient (Ef-Ob) or inefficient (In-Ob) with respect to fatty acid oxidation (FAO). Here, we sought to determine if this was due to a primary defect in FAO. Accordingly, we measured FAO in myogenic differentiating MSCs under three conditions: 1) myogenesis alone, 2) excess fatty acid exposure, and 3) excess fatty acid exposure plus a chemical uncoupler to increase metabolic rate. Compared to NW and Ef-Ob MSCs, In-Ob displayed lower FAO in myogenesis alone and after fatty acid plus uncoupler, indicating In-Ob were less metabolically flexible after increasing lipid availability and metabolic rate, demonstrating a primary deficit in FAO. MSC FAO was negatively associated with fasting maternal glucose and insulin, and positively associated with fasting HDL-cholesterol. MSC FAO was negatively associated with infant fat mass. These data indicate a less favorable maternal metabolic milieu, independent of maternal BMI, reduces intrinsic MSC FAO and is linked to higher infant adiposity as early as birth.
... Previous literature from high-and middle-income countries presents a heterogeneous picture of the impact of HFDP on childhood BMI. While some studies have found an independent effect of HFDP on BMI and overweight/obesity (Nehring et al. 2013;Hillier et al. 2016;Zhu et al. 2016;Grunnet et al. 2017;Tam et al. 2017;Wang et al. 2018;Gu et al. 2019), others showed no significant association (Pettitt et al. 2010;Pham et al. 2013;Bider-Canfield et al. 2017;Kaseva et al. 2018;Kearney et al. 2018;Lowe et al. 2018;Pitchika et al. 2018). Interestingly, some studies found a significant association in school-aged children and adolescents that was not evident in earlier childhood (Pettitt et al. 2010;Crume et al. 2011;Zhu et al. 2016), possibly due to the accumulation of environmental and behavioural risks for obesity throughout childhood (Silverman et al. 1991;Crume et al. 2011). ...
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Background: Understanding the association between maternal metabolic conditions in pregnancy and the risk of childhood overweight, a growing concern in sub-Saharan Africa (SSA), helps to identify opportunities for childhood obesity prevention. Aim: To assess the association between hyperglycaemia first detected in pregnancy (HFDP) (gestational diabetes mellitus [GDM] and diabetes in pregnancy [DIP]) and child obesity and adiposity in pre-school-aged children in South Africa, independently of maternal BMI. Subjects and methods: Measurement of anthropometry and fat mass index (FMI) by the deuterium dilution method was done for 102 3-6-year-old children born to mothers with HFDP and 102 HFDP-unexposed children. Hierarchical regression analysis and generalised structural equation modelling (GSEM) were performed. Results: The prevalence of overweight/obesity was 10.5% and 11.1% in children exposed to GDM and DIP, respectively, and 3.9% in the HFDP-unexposed group. Log-transformed FMI was significantly higher in the DIP-exposed group (β = 0.166, 95% CI = 0.014-0.217 p= .026), but not when adjusting for maternal pregnancy BMI (β = 0.226, 95% CI = 0.003-0.015, p = .004). GSEM showed significant total effects of maternal BMI and birth weight on FMI/BMI. Conclusions: Maternal pregnancy BMI seems to play a greater role in the development of childhood adiposity than maternal hyperglycaemia, requiring further research and identifying maternal BMI as a relevant prevention target in our setting.
... Compelling evidence has shown that maternal hyperglycemia and diabetes may affect offspring risk of obesity beginning in childhood (3)(4)(5)(6)(7). In particular, maternal glucose levels during pregnancy, ranging from normal to gestational diabetes mellitus (GDM), have been consistently related to childhood obesity (8)(9)(10)(11). ...
Article
Objective The purpose of this study was to estimate the associations of genetically determined maternal blood glucose levels with obesity‐related outcomes among children from pregnancies with and without gestational diabetes mellitus (GDM). Methods A total of 1,114 mothers with (N = 560) and without (N = 554) GDM and their children were included in the present study. A maternal genetic risk score (GRS) for blood glucose was constructed on the basis of 17 single‐nucleotide polymorphisms identified from a recent genome‐wide association study. Results It was found that maternal GRS for blood glucose showed different associations with offspring risk of overweight and obesity, as well as adiposity measures (all P for interaction < 0.05). Among mothers without GDM, genetically determined maternal blood glucose levels were associated with an 89% higher risk of overweight in their children (95% CI: 42%‐152% per SD increase in GRS, P = 1.40 × 10⁻⁵) and a 120% higher risk of obesity (44%‐235%, P = 2.61 × 10⁻⁴) after adjustment for covariates. In addition, higher maternal GRS for blood glucose was associated with children's increased obesity‐related traits (all P < 0.05). However, no significant associations were observed among children of mothers with GDM. Conclusions This study indicates that GDM status may modify the relation between genetically determined glucose levels and obesity risk among children.
... Recent studies show that the investigations conducted by Lowe et al, 15 Hillier et al., 24 and Skrypnik et al. 25 demonstrate a significant relationship between maternal GDM and childhood obesity; whereas in some other studies, this relationship remained weak. [14][15] Most of these studies were conducted in high-income countries, and many of them are cross-sectional. ...
Article
Background: Recently, childhood obesity has become one of the most serious public health problems in the world. Gestational diabetes mellitus (GDM) is considered a risk factor for childhood overweight and obesity. The study aimed at investigating the relationship between maternal GDM and childhood obesity in children aged from 1 to 3 years. Methods: In this retrospective cohort study, 237 GDM and 296 non-GDM mothers and their offspring who were followed up by Family Medicine Clinics in Rize province of Turkey were assessed. World Health Organization (WHO) criteria were used for the diagnosis of maternal GDM. Crude and adjusted logistic regression models were calculated for the association of gestational diabetes and childhood overweight/obesity. Gender and age-specific percentile tables were used for the categorization of BMI. Results: Statistical analysis carried out with adjustment for potential confounders (mother's age, educational status, smoking status, BMI, gestational weight gain, children's gender, and gestational birth weight) provided results with an odds ratio of 2.99; 95% CI 1.14-7.94 and 7.77; 95% CI 1.92-31.37 for the impact of gestational diabetes on childhood overweight and obesity at 2 and 3 years of age, respectively. Conclusions: This study found evidence for maternal GDM to cause the risk of early childhood obesity. Therefore, proper intervention strategies are required for this high-risk population.
... Moreover, EGWG may have longer-term consequences in offspring. It has been associated with greater offspring BMI and higher systolic blood pressure in early adulthood as well as obesity in the first decade of life (41,42). Hillier et al. found that the attributable risk for childhood obesity was 16.4% for excessive gestational weight gain (41). ...
... It has been associated with greater offspring BMI and higher systolic blood pressure in early adulthood as well as obesity in the first decade of life (41,42). Hillier et al. found that the attributable risk for childhood obesity was 16.4% for excessive gestational weight gain (41). In addition, Sridhar el al. reported that excessive gestational weight gain was associated with 46% increase in odds of having overweight/obesity at 2-5 years, independent of gestational diabetes (43). ...
... Obesity is a well-recognized risk factor for PGD and GD. Diabetes as well as increased maternal BMI are recognized risk factors for macrosomia, as well as for overweight/obesity at a young age and type 2 diabetes in the offspring (41,59). This may be a vicious cycle as these obese offspring may propagate an abnormal metabolic environment in utero during gestation (60,61). ...
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Objective: To evaluate the risk of macrosomia in newborns from women with gestational diabetes, pregestational diabetes, overweight, and obesity in Uruguay in 2012, as well as its association with prolonged pregnancy, maternal age, multiparity, and excessive gestational weight gain (EGWG). Methods: We performed a cross-sectional study of 42,663 pregnant women. The risk of macrosomia was studied using logistic regression. Results: Mean maternal age was 26.7 ± 6.8 years. Pregestational overweight and obesity was present in 20.9% and 10.7% of women, respectively. There were 28.1% and 19.8% of women overweight and obese at the end of the pregnancy, respectively. Furthermore, 0.5% had pregestational diabetes and 8.5% were multiparous. Twenty two percent developed gestational diabetes and 44.9% had EGWG. The prevalence of macrosomia was 7.9%, significantly more prevalent in males (10.0% vs. 5.5%, p<0.005). Univariate analysis showed that obesity and overweight pre-pregnancy, obesity and overweight at the end of pregnancy, EGWG, pregestational diabetes, gestational diabetes, multiparity, prolonged pregnancy, and male newborn were strongly associated with macrosomia (p<0.0001). Maternal age >35 years did not increase the risk of macrosomia. After multiple logistic regression macrosomia was more likely in pre-gestational obese women (OR 1.24; CI 1.07-1.44), overweight women at the end of pregnancy (OR 1.66; CI 1.46-1.87), obese women at the end of pregnancy (OR 2.21; CI 1.90-2.58), women with EGWG (OR 1.78; CI 1.59-1.98), pregestational diabetes (OR 1.75; CI 1.15-2.69), gestational diabetes (OR 1.39; CI 1.25-1.53), prolonged pregnancy (OR 2.67; CI 2.28-3.12), multiparity (OR 1.24; CI 1.04-1.48), and male newborn (OR 1.89; CI 1.72-2.08). Conclusion: Maternal overweight, obesity, EGWG, and gestational diabetes are prevalent in Uruguay, increasing the risk of macrosomia. Efforts to implement strategies to decrease the prevalence of overweight and obesity among women of reproductive age are essential to improve maternal and neonatal outcomes.