Risk Of Obesity In Offspring Research Articles

Gestational diabetes mellitus: risks and management during and after pregnancy.

Gestational diabetes mellitus (GDM) carries a small but potentially important risk of adverse perinatal outcomes and a long-term risk of obesity and glucose intolerance in offspring. Mothers with GDM have an excess of hypertensive disorders during pregnancy and a high risk of developing diabetes mellitus thereafter. Diagnosing and treating GDM can reduce perinatal complications, but only a small fraction of pregnancies benefit. Nutritional management is the cornerstone of treatment; insulin, glyburide and metformin can be used to intensify treatment. Fetal measurements complement maternal glucose monitoring in the identification of pregnancies that require such intensification. Glucose testing shortly after delivery can stratify the short-term diabetes risk in mothers. Thereafter, annual glucose and HbA(1c) testing can detect deteriorating glycaemic control, a harbinger of future diabetes mellitus, usually type 2 diabetes mellitus. Interventions that mitigate obesity or its metabolic effects are most potent in preventing or delaying diabetes mellitus. Lifestyle modification is the primary approach; use of medications for diabetes prevention after GDM remains controversial. Family planning enables optimization of health in subsequent pregnancies. Breastfeeding may reduce obesity in children and is recommended. Families should be encouraged to help children adopt lifestyles that reduce the risk of obesity.

Cesarean section might moderately increase offspring obesity risk

Cesarean section might moderately increase offspring obesity risk

Effect of reducing the n−6:n−3 long-chain PUFA ratio during pregnancy and lactation on infant adipose tissue growth within the first year of life: an open-label randomized controlled trial

The composition of long-chain PUFAs (LCPUFAs) in the maternal diet may affect obesity risk in the mother's offspring. We hypothesized that a reduction in the n-6 (omega-6):n-3 (omega-3) LCPUFA ratio in the diet of pregnant women and breastfeeding mothers may prevent expansive adipose tissue growth in their infants during the first year of life. In a randomized controlled trial, 208 healthy pregnant women were randomly assigned to an intervention (1200 mg n-3 LCPUFAs as a supplement per day and a concomitant reduction in arachidonic acid intake) or a control diet from the 15th wk of pregnancy to 4 mo of lactation. The primary outcome was infant fat mass estimated by skinfold thickness (SFT) measurements at 4 body sites at 3-5 d, 6 wk, and 4 and 12 mo postpartum. Secondary endpoints included sonographic assessment of abdominal subcutaneous and preperitoneal fat, fat distribution, and child growth. Infants did not differ in the sum of their 4 SFTs at ≤1 y of life [intervention: 24.1 ± 4.4 mm (n = 85); control: 24.1 ± 4.1 mm (n = 80); mean difference: -0.0 mm (95% CI: -1.3, 1.3 mm)] or in growth. Likewise, longitudinal ultrasonography showed no significant differences in abdominal fat mass or fat distribution. We showed no evidence that supplementation with n-3 fatty acids and instructions to reduce arachidonic acid intake during pregnancy and lactation relevantly affects fat mass in offspring during the first year of life. Prospective long-term studies are needed to explore the efficacy of this dietary approach for primary prevention. This trial was registered at clinicaltrials.gov as NCT00362089.

Impact of Maternal Physical Activity and Infant Feeding Practices on Infant Weight Gain and Adiposity

Increasing evidence supports the contribution of intrauterine environmental exposures on obesity risk in offspring. Few studies have included maternal and infant lifestyle factors. Our objective was to study the impact of maternal physical activity, infant feeding, and screen time on offspring weight gain and adiposity. In a prospective cohort study, 246 mothers underwent testing during pregnancy to assess glucose tolerance status and insulin sensitivity. Anthropometry and questionnaires on physical activity, infant feeding, and screen time were completed. Multiple-linear regression was performed to examine the impact of maternal and infant factors on infant weight gain and weight-for-length z-score at 1 year. Infant weight outcomes were negatively predicted by maternal pregravid vigorous/sport index and exclusive breastfeeding duration. After adjustment, each unit increase in maternal pregravid vigorous/sport index decreased infant weight gain by 218.6 g (t = 2.44, P = 0.016) and weight-for-length z-score by 0.20 (t = 2.17, P = 0.031). Each month of exclusive breastfeeding reduced infant weight gain by 116.4 g (t = 3.97, P < 0.001) and weight-for-length z-score by 0.08 (t = 2.59, P = 0.01). Maternal pregravid physical activity and exclusive breastfeeding duration are associated with weight gain and adiposity as early as 1 year of age.

The Effect of Neonatal Leptin Antagonism in Male Rat Offspring Is Dependent upon the Interaction between Prior Maternal Nutritional Status and Post-Weaning Diet

Epidemiological and experimental studies report associations between overweight mothers and increased obesity risk in offspring. It is unclear whether neonatal leptin regulation mediates this association between overweight mothers and offspring obesity. We investigated the effect of neonatal treatment with a leptin antagonist (LA) on growth and metabolism in offspring of mothers fed either a control or a high fat diet. Wistar rats were fed either a control (CON) or a high fat diet (MHF) during pregnancy and lactation. Male CON and MHF neonates received either saline (S) or a rat-specific pegylated LA on days 3, 5, and 7. Offspring were weaned onto either a control or a high fat (hf) diet. At day 100, body composition, blood glucose, β-hydroxybutyrate and plasma leptin and insulin were determined. In CON and MHF offspring, LA increased neonatal bodyweights compared to saline-treated offspring and was more pronounced in MHF offspring. In the post-weaning period, neonatal LA treatment decreased hf diet-induced weight gain but only in CON offspring. LA treatment induced changes in body length, fat mass, body temperature, and bone composition. Neonatal LA treatment can therefore exert effects on growth and metabolism in adulthood but is dependent upon interactions between maternal and post-weaning nutrition.

Lifecourse approach to racial/ethnic disparities in childhood obesity.

Eliminating racial/ethnic disparities in health and health care is a national priority, and obesity is a prime target. During the last 30 y in the United States, the prevalence of obesity among children has dramatically increased, sparing no age group. Obesity in childhood is associated with adverse cardio-metabolic outcomes such as hypertension, hyperlipidemia, and type II diabetes and with other long-term adverse outcomes, including both physical and psychosocial consequences. By the preschool years, racial/ethnic disparities in obesity prevalence are already present, suggesting that disparities in childhood obesity prevalence have their origins in the earliest stages of life. Several risk factors during pregnancy are associated with increased risk of offspring obesity, including excessive maternal gestational weight gain, gestational diabetes, smoking during pregnancy, antenatal depression, and biological stress. During infancy and early childhood, rapid infant weight gain, infant feeding practices, sleep duration, child's diet, physical activity, and sedentary practices are associated with the development of obesity. Studies have found substantial racial/ethnic differences in many of these early life risk factors for childhood obesity. It is possible that racial/ethnic differences in early life risk factors for obesity might contribute to the high prevalence of obesity among minority preschool-age children and beyond. Understanding these differences may help inform the design of clinical and public health interventions and policies to reduce the prevalence of childhood obesity and eliminate disparities among racial/ethnic minority children.

266: The risk of childhood obesity in toddler offspring of gestational diabetic mothers

266: The risk of childhood obesity in toddler offspring of gestational diabetic mothers

Abstract 18063: Maternal and Postnatal High-Fat Diet Interaction Leads to Greater Risk of Myocardial Dysfunction in Offspring via Obesity-Induced Lipotoxicity, IRS-1 Serine Phosphorylation and Mitochondrial Defects

Introduction: Maternal obesity/overnutrition during gestation and lactation are associated with increased prevalence of obesity and cardiovascular risk in adult offspring. Given the pervasive “obesogenic” environment, long-term consequences of maternal and/or postnatal overnutrition on myocardial function warrant immediate attention. Objective: We examined the impact of maternal and long- term postnatal dietary fat exposure on metabolic, myocardial, intracellular Ca2+, insulin and mitochondrial responses. Methods and Results: Pregnant FVB mice were fed either a low-fat (LF, 10% of calories) or high-fat (HF, 45% of calories) diet during gestation and lactation. Weaning male offspring were randomized and placed on either LF or HF (a food-restricted HF-fed mice served as weight control group) for 4 months prior to assessment of metabolic indexes, myocardial histology, cardiac function, insulin signaling, mitochondrial integrity and ROS generation. Compared with LF-fed and HF-fed weight-control mice, postnatal HF intake resulted in obesity (DIO), exhibited marked dyslipidemia, blunted insulin sensitivity, cardiac hypertrophy, compromised myocardial function, intracellular Ca2+ homeostasis and mitochondrial biogenesis, all of which were significantly accentuated in postnatal HF-fed mice with maternal high fat exposure.Interestingly, LF-fed offspring from HF-fed dams displayed higher body weights, increased adiposity and dampened insulin sensitivity compared to LF-fed controls. Maternal HF exposure upregulated postnatal HF-induced IRS-1 serine phosphorylation, PTP1B, lipogenic enzyme SCD-1 and hypertrophic markers while downregulating cardiac AMPK signaling and PGC-1α. Importantly, myocardial and mitochondrial ultrastructural abnormalities were more pronounced in HF-fed offspring with maternal HF exposure, as shown by loss of mitochondrial density and membrane potential, increased ROS generation and apoptosis. Conclusion: We conclude that prenatal fat exposure may program the offspring at a higher risk for postnatal DIO induced cardiac hypertrophy and dysfunction possibly related to cardiac hypertrophy and lipotoxicity, impaired insulin signaling, mitochondrial dysfunction and oxidative stress.

Maternal Cigarette Smoke Exposure Contributes to Glucose Intolerance and Decreased Brain Insulin Action in Mice Offspring Independent of Maternal Diet

BackgroundMaternal smoking leads to intrauterine undernutrition and is associated with low birthweight and higher risk of offspring obesity. Intrauterine smoke exposure (SE) may alter neuroendocrine mediators regulating energy homeostasis as chemicals in cigarette smoke can reach the fetus. Maternal high-fat diet (HFD) consumption causes fetal overnutrition; however, combined effects of HFD and SE are unknown. Thus we investigated the impact of combined maternal HFD and SE on adiposity and energy metabolism in offspring.MethodFemale Balb/c mice had SE (2 cigarettes/day, 5 days/week) or were sham exposed for 5 weeks before mating. Half of each group was fed HFD (33% fat) versus chow as control. The same treatment continued throughout gestation and lactation. Female offspring were fed chow after weaning and sacrificed at 12 weeks.ResultsBirthweights were similar across maternal groups. Faster growth was evident in pups from SE and/or HFD dams before weaning. At 12 weeks, offspring from HFD-fed dams were significantly heavier than those from chow-fed dams (chow-sham 17.6±0.3 g; chow-SE 17.8±0.2 g; HFD-sham 18.7±0.3 g; HFD-SE 18.8±0.4 g, P<0.05 maternal diet effect); fat mass was significantly greater in offspring from chow+SE, HFD+SE and HFD+sham dams. Both maternal HFD and SE affected brain lactate transport. Glucose intolerance and impaired brain response to insulin were observed in SE offspring, and this was aggravated by maternal HFD consumption.ConclusionWhile maternal HFD led to increased body weight in offspring, maternal SE independently programmed adverse health outcomes in offspring. A smoke free environment and healthy diet during pregnancy is desirable to optimize offspring health.

Maternal Obesity Promotes a Proinflammatory Signature in Rat Uterus and Blastocyst

Maternal obesity at conception increases the risk of offspring obesity, thus propagating an intergenerational vicious cycle. Male offspring born to obese dams are hyperresponsive to high fat-diets, gaining greater body weight, fat mass, and additional metabolic sequelae compared to lean controls. In this report, we identify the impact of maternal obesity before conception, on the embryo, and intrauterine milieu during the periimplantation period. We conducted global transcriptomic profiling in the uterus and periimplantation blastocyst, gene/protein expression analyses of inflammatory pathways in conjunction with endocrine and metabolic characterization in the dams at implantation. Uterine gene expression profiles of lean and obese dams revealed distinct signatures for genes regulating inflammation and lipid metabolism. Both pathway and gene-set enrichment analysis revealed uterine nuclear factor-κB and c-Jun N-terminal kinase signaling to be up-regulated in the uterus of obese dams, which was confirmed via immunoblotting. Obese uteri also evidenced an inflammatory secretome with higher chemokine mRNA abundance (CCL2, CCL5, CCL7, and CxCL10) and related regulators (TLR2, CD14, and Ccr1). Increased inflammation in the uterus was associated with ectopic lipid accumulation and expression of lipid metabolic genes. Gene expression in sex-identified male periimplantation blastocyst at day postcoitum 4.5 was clearly influenced by maternal obesity (359 transcripts, ±1.4-fold), including changes in developmental and epigenetic regulators. Akin to the uterus, nuclear factor-κB-regulated proinflammatory genes (CCL4 and CCL5) increased and expression of antioxidant (GPx3) and mitochondrial (TFAM and NRF1) genes decreased in the obese embryos. Our results suggest that ectopic lipid and inflammation may link maternal obesity to increased predisposition of offspring to obesity later in life.

Parental smoking during pregnancy, early growth, and risk of obesity in preschool children: the Generation R Study

Maternal smoking during pregnancy seems to be associated with obesity in offspring. Not much is known about the specific critical exposure periods or underlying mechanisms for this association. We assessed the associations of active maternal and paternal smoking during pregnancy with early growth characteristics and risks of overweight and obesity in preschool children. This study was a population-based, prospective cohort study from early fetal life until the age of 4 y in 5342 mothers and fathers and their children. Growth characteristics [head circumference, length, weight, and body mass index (BMI; in kg/m(2))] and overweight and obesity were repeatedly measured at the ages of 1, 2, 3, and 4 y. In comparison with children from nonsmoking mothers, children from mothers who continued smoking during pregnancy had persistently smaller head circumferences and heights until the age of 4 y, whereas their weights were lower only until the age of 3 mo. This smaller length and normal to higher weight led to an increased BMI [SD score difference: 0.11; 95% CI: 0.02, 0.20; P < 0.05)] and an increased risk of obesity (odds ratio: 1.61; 95% CI: 1.03, 2.53; P < 0.05) at the age of 4 y. In nonsmoking mothers, paternal smoking was not associated with postnatal growth characteristics or risk of obesity in offspring. Maternal smoking during pregnancy was associated with a higher BMI at the age of 4 y in children with a normal birth weight and in those who were small for gestational age at birth. Our findings suggest that direct intrauterine exposure to smoke until late pregnancy leads to different height and weight growth adaptations and increased risks of overweight and obesity in preschool children.

Maternal Obesity and Developmental Programming of Metabolic Disorders in Offspring: Evidence from Animal Models

The incidence of obesity and overweight has reached epidemic proportions in the developed world as well as in those countries transitioning to first world economies, and this represents a major global health problem. Concern is rising over the rapid increases in childhood obesity and metabolic disease that will translate into later adult obesity. Although an obesogenic nutritional environment and increasingly sedentary lifestyle contribute to our risk of developing obesity, a growing body of evidence links early life nutritional adversity to the development of long-term metabolic disorders. In particular, the increasing prevalence of maternal obesity and excess maternal weight gain has been associated with a heightened risk of obesity development in offspring in addition to an increased risk of pregnancy-related complications. The mechanisms that link maternal obesity to obesity in offspring and the level of gene-environment interactions are not well understood, but the early life environment may represent a critical window for which intervention strategies could be developed to curb the current obesity epidemic. This paper will discuss the various animal models of maternal overnutrition and their importance in our understanding of the mechanisms underlying altered obesity risk in offspring.

Gestational Diabetes Mellitus and Risk of Childhood Overweight and Obesity in Offspring: A Systematic Review

We systematically reviewed research examining the association between gestational diabetes (GDM) and childhood overweight and obesity. We identified studies from three sources: (1) a PubMed search of articles published between January 1990–January 2011, (2) reference lists of publications from the PubMed search, and (3) reference lists of review articles. We included studies that examined GDM separately from pregestational diabetes and childhood overweight or obesity defined as BMI > 85th or 95th percentile. A total of 12 studies were included in the systematic review. Crude odds ratios for the relationship between GDM and childhood overweight or obesity ranged from 0.7 to 6.3; in 8 studies, the associations were not statistically significant. In only 3 studies were results adjusted for any confounders; in the 2 that adjusted for prepregnancy obesity, the GDM and childhood overweight or obesity associations were attenuated and not statistically significant after adjustment. This paper demonstrates inconsistent evidence of an association between GDM and offspring overweight and obesity due to the methodological limitations of existing studies. Recommendations for future research are presented, which address methodological challenges.

Maternal Diabetes in Pregnancy: Early and Long-Term Outcomes on the Offspring and the Concept of “Metabolic Memory”

The adverse outcomes on the offspring from maternal diabetes in pregnancy are substantially documented. In this paper, we report main knowledge on impacts of maternal diabetes on early and long-term health of the offspring, with specific comments on maternal obesity. The main adverse outcome on progenies from pregnancy complicated with maternal diabetes appears to be macrosomia, as it is commonly known that intrauterine exposure to hyperglycemia increases the risk and programs the offspring to develop diabetes and/or obesity at adulthood. This “fetal programming”, due to intrauterine diabetic milieu, is termed as “metabolic memory”. In gestational diabetes as well as in macrosomia, the complications include metabolic abnormalities, degraded antioxidant status, disrupted immune system and potential metabolic syndrome in adult offspring. Furthermore, there is evidence that maternal obesity may also increase the risk of obesity and diabetes in offspring. However, women with GDM possibly exhibit greater macrosomia than obese women. Obesity and diabetes in pregnancy have independent and additive effects on obstetric complications, and both require proper management. Management of gestational diabetes mellitus and maternal obesity is essential for maternal and offspring's good health. Increasing physical activity, preventing gestational weight gain, and having some qualitative nutritional habits may be beneficial during both the pregnancy and offspring's future life.

Maternal Behaviors during Pregnancy Impact Offspring Obesity Risk

This study investigated the effects of maternal changes during pregnancy in diet, exercise, and psychosocial factors on offspring weight parameters at birth and 6 months. In overweight/obese (OW/OB; n = 132) mothers, greater % kcal from sweets early in pregnancy was the strongest, independent predictor of higher weight for age (WFA) (beta = 0.19; P = 0.004), higher odds of macrosomia (OR = 1.1 (1.0–1.2); P = 0.004) andWFA >90th percentile at birth (OR = 1.2 (1.1–1.3); P = 0.002) and higher WFA at 6 months (beta = 0.30; P = 0.002). In normal weight (n = 153) mothers, higher intake of soft drinks was the strongest predictor of higher offspring WFA at birth (beta = 0.16; P = 0.04) but not at 6 months. Prenatal physical activity, depressive symptoms, and sleep-related variables did not significantly predict offspring weight outcomes. Mothers' eating behaviors during pregnancy, especially intake of sweets in OW/OB mothers, may have a lasting effect on child weight.

Prenatal nutritional influences on obesity risk in offspring

The incidence of obesity and overweight has almost doubled in Western societies over the last 2 decades, a trend mirrored in developing nations transitioning to first-world economies. Obesity is strongly associated with the comorbidities of type 2 diabetes, hyperten- sion, and heart disease and represents an enormous burden to health care systems. Of even more concern is the increase of around 40% in the prevalence of childhood obesity and type 2 diabetes over the last 20 years. Metabolic disease results from complex interactions of many factors, including genetic, physiologic, behavioral, and environmental influences. The recent rate at which these diseases have increased suggests that environmental, eg, epigenetic, and behavioral influences, rather than genetic causes, are fuelling the present epidemic. In this context, the developmental origins of health and disease hypothesis has highlighted the link between periconceptual, fetal, and early infant phases of life and the subsequent development of adult obesity and related metabolic disorders. Both maternal undernutrition (global and tar- geted) and maternal obesity elicit an obese offspring phenotype. This review will examine the role of altered maternal nutrition on obesity risk in offspring, the interactions with the postnatal nutritional environment, the possible strategies for intervention, and the role of epigenetics in the disease process.

Associations Between Mothers' and Their Children's Weights at 4 Years of Age

OBJECTIVES: To examine the importance of maternal weight characteristics as predictors of overweight (BMI ≥85th percentile and <95th percentile) and obesity (BMI ≥ 95th percentile) in offspring at age 4 years. METHODS: Chi-square and logistic regression analyses were conducted on a sample of 321 mother/child pairs from an earlier observational cohort study on mothers' postpartum weight retention. RESULTS: Maternal early pregnancy BMI and infant birth weight were each positively and significantly (p <0.05) associated with increased risk of obesity in offspring at age 4 years. A significant interaction was found between these two variables in predicting children's risk of obesity. It was driven by the high proportion of obese children among obese women who had infants weighing < 3 kg at birth. Net gestational weight gain was not associated with obesity risk in children, but was positively associated with infant birth weight among normal weight and overweight women. CONCLUSIONS: Reducing maternal BMI in the preconception period among overweight and obese women and preventing excessive weight gain in pregnancy for all women appear to be appropriate strategies to address the childhood obesity epidemic.

Impact of maternal obesity on offspring obesity and cardiometabolic disease risk

The prevalence of obesity among pregnant women is increasing. In addition to the short-term complications of obesity during pregnancy in both mother and child, it is now recognised that maternal obesity has long-term adverse outcomes for the health of her offspring in later life. Evidence from both animal and human studies indicates that maternal obesity increases the risk for the offspring in developing obesity and altering body composition in child- and adulthood and, additionally, it also has an impact on the offspring's cardiometabolic health with dysregulation of metabolism including glucose/insulin homoeostasis, and development of hypertension and vascular dysfunction. Potential mechanisms include effects on the development and function of adipose tissue, pancreas, muscle, liver, the vasculature and the brain. Further studies are required to elucidate the mechanisms underpinning the programming of disease risk in the offspring as a consequence of maternal obesity. The ultimate aim is to identify potential targets, which may be amenable to prevention or early intervention in order to improve the health of this and future generations.

Maternal high fat feeding and gestational dietary restriction: Effects on offspring body weight, food intake and hypothalamic gene expression over three generations in mice

Excessive gestational weight gain and maternal obesity have both been associated with increased incidence of obesity and metabolic disorder in offspring in both humans and animal models. The objectives of this study were to determine (1) whether mild gestational food restriction during the third trimester (GFR) would alter food intake and growth parameters of offspring, (2) whether effects of GFR depended on diet (high fat [HF] vs chow), (3) whether effects of excessive gestational weight gain (WG) would become magnified across generations, and (4) whether diet and GFR would alter hypothalamic gene expression in adult offspring. Three generations of female C57BL/6 mice were fed chow or HF diet, mated at 11 weeks of age and assigned to ad libitum feeding or 25% GFR. Offspring were fed the same diet as their mothers. Results showed (1) maternal gestational WG was positively correlated with offspring WG. (2) HF offspring weighed less ( p < 0.01) at weaning (WWT) but gained more during the 8 weeks after weaning than chow-fed offspring ( p < 0.05), resulting in higher final body weights (BW) ( p < 0.01). (3) HF males from GFR mothers had higher WWT ( p < 0.05), but subsequent WG and final BW were less ( p < 0.05) compared to males from ad lib mothers. (4) In the HF group, GFR also resulted in decreased FI ( p < 0.05) and FE ( p < 0.07) in offspring, compared to offspring from ad lib mothers. (5) In generation 3, hypothalamic expression of tyrosine hydroxylase was lower in HF males from GFR mothers compared to HF males from ad lib mothers ( p < 0.05). In conclusion, gender and maternal GFR had independent effects on growth and FI, and hypothalamic gene expression was dependent on both gender and maternal GFR in HF offspring. Even mild food restriction of obese mothers during pregnancy may have beneficial effects in reducing the risk or degree of obesity in offspring.

Association of existing diabetes, gestational diabetes and glycosuria in pregnancy with macrosomia and offspring body mass index, waist and fat mass in later childhood: findings from a prospective pregnancy cohort

The aim of the study was to examine the association of existing diabetes (i.e. already diagnosed prior to pregnancy), gestational diabetes and glycosuria (both diagnosed and ascertained during pregnancy) with birthweight and future offspring BMI, waist circumference and fat mass (assessed by dual x-ray emission absorptiometry). A prospective pregnancy/birth cohort study was performed using data from the Avon Longitudinal Study of Parents and Children. Among 10,591 mother-offspring pairs included in analyses with birth size, women with existing diabetes (n = 40), those diagnosed with gestational diabetes (n = 53) and those with at least two episodes of ++ glycosuria (n = 372) had greater mean birthweight and odds for macrosomia (birthweight > 4,000 g) than women with none of these. Adjusted odds ratios for macrosomia were 3.56 (95% CI 1.53-8.28), 5.50 (95% CI 1.18-10.30) and 1.58 (95% CI 1.18-2.12) for existing diabetes, gestational diabetes and glycosuria, respectively. Among 6,842 mother-offspring pairs with anthropometric measurements at age 9-11 years, maternal gestational diabetes and glycosuria (but not existing diabetes) were associated with increased offspring odds of general or central overweight/obesity. For gestational diabetes, these associations attenuated towards the null with adjustment for maternal prepregnancy BMI, but independent associations remained for glycosuria. The adjusted odds ratio for general overweight/obesity when comparing women with at least two episodes of ++ glycosuria with those with no evidence of diabetes or glycosuria was 1.35 (95% CI 1.00-1.82) and that for central obesity (top 10% waist circumference vs all others) was 1.31 (95% CI 1.00-1.72). These results provide some evidence for a long-term effect of maternal glycaemia in pregnancy on offspring obesity risk.