Children Of Diabetic Mothers Research Articles

Dapagliflozin Mitigated Elevated Disomic and Diploid Sperm in a Mouse Model of Diabetes and Recover the Disrupted Ogg1, Parp1, and P53 Gene Expression.

Increases in numerical chromosomal syndromes were observed in children of diabetic mothers. However, the effects of diabetes on male reproduction, specifically numerical chromosomal aberrations (aneuploidy), have not been studied. Furthermore, despite the increasing use of dapagliflozin for diabetes treatment, no data exists on its ability to affect aneuploidy levels in germ cells. Thus, our investigation aimed to evaluate the effects of diabetes on spontaneous sperm aneuploidy and whether treatment with dapagliflozin influences the frequency of aneuploidy in the sperm of an experimental diabetic animal model. Our findings show that dapagliflozin has no aneugenic effects on the meiotic stages of spermatogenesis. In contrast, diabetes raised the frequency of aneuploidy, and dapagliflozin administration decreased the elevated levels of disomic and diploid sperm. The level of oxidative stress was markedly increased in diabetic mice, but were reduced by dapagliflozin treatment. Furthermore, the expression of some of DNA repair genes was disrupted in diabetic animals, whereas dapagliflozin therapy restored these disruptions and significantly enhanced DNA repair. Thus, dapagliflozin may effectively ameliorate diabetes-induced aneugenic effects on male meiosis and treating diabetic patients with dapagliflozin may effectively mitigate the transmission of diabetes-induced chromosomal defects to offspring.

Hyperglycemia affects neuronal differentiation and Nestin, FOXO1, and LMO3 mRNA expression of human Wharton's jelly mesenchymal stem cells of children from diabetic mothers

Pregestational Diabetes Mellitus (PDM) during pregnancy constitutes an unfavorable embryonic and fetal development environment, with a high incidence of congenital malformations (CM). Neural tube defects are the second most common type of CM in children of diabetic mothers (CDM), who also have an elevated risk of developing neurodevelopmental disorders. The mechanisms that lead to these neuronal disorders in CDM are not yet fully understood. The present study aimed to know the effect of hyperglycemia on proliferation, neuronal differentiation percentage, and expression of neuronal differentiation mRNA markers in human umbilical cord Wharton's jelly mesenchymal stem cells (hUCWJMSC) of children from normoglycemic pregnancies (NGP) and PDM. We isolated and characterized hUCWJMSC by flow cytometry, immunofluorescence, RT-PCR and were induced to differentiate into adipocytes, osteocytes, and neurons. Proliferation assays were performed to determine the doubling time, and Nestin, TUBB3, FOXO1, KCNK2, LMO3, and MAP2 mRNA gene expression was assessed by semiquantitative RT-PCR. Hyperglycemia significantly decreased proliferation and neuronal differentiation percentage in NGP and PDM cells treated with 40 mM d-glucose. Nestin mRNA expression decreased under control glycemic conditions, while FOXO1, KCNK2, LMO3, and MAP2 mRNA expression increased during neuronal differentiation in both NGP and PDM cells. On the other hand, under hyperglycemic conditions, Nestin was significantly decreased in cells from NGP but not in cells from PDM, while mRNA expression of FOXO1 and LMO3 was significantly increased in cells from NGP, but not in cells from PDM. We found evidence that maternal PDM, with hyperglycemia in culture, affects the biological properties of fetal cells. All these results could be part of fetal programming.

Motor Developmental Outcomes in Children Exposed to Maternal Diabetes during Pregnancy: A Systematic Review and Meta-Analysis.

Studies on the association of maternal diabetes with motor development in children provide inconsistent findings. We searched MEDLINE/PubMed, EMBASE, Emcare, PsycINFO, and Google Scholar databases for primary observational, case–control, or cohort studies that report on the motor development of children exposed to maternal diabetes during pregnancy. Quality appraisal and data extraction were performed independently and in duplicate. A meta-analysis of summary measures was performed using random-effect models. Eighteen studies were identified for inclusion, however, only 13 were included in the meta-analysis. Exposure to maternal diabetes during pregnancy was associated with a lower pooled motor development in children and a decrease in both gross and fine motor development. Among all other factors, pre-existing diabetes and other gestational comorbidities, such as hypertension and obesity, or low socioeconomic status, also affect child development. Therefore, among children of diabetic mothers, those with other gestational comorbidities or pre-existing diabetes were more likely to be at risk developmentally.

Hipokalcemija novorođenčeta usled transfuzije eritrocita - prikaz slučaja

Introduction: Hypocalcemia in preterm infants could occurs as early or late. Causes of late onset of hypocalcaemia: maternal vitamin D deficiency, metabolic syndromes, congenital abnormalities, iatrogenic (transfusion, bicarbonate therapy, phototherapy, antibiotics). Case report: The authors describe the occurrence of late hypocalcemia following transfusion of erythrocytes to the second newborn from a twin pregnancy born prematurely in the 32/33 week of gestation. Mother is diabetic and has hypertension, edema, hypothyroidism, and preeclampsia during pregnancy. Due to the detected pyelectasis in newborn, prophylactic use of cephalexin was introduced. At the end of the first month of life, anemia appear indicating a transfusion. The infant received 50 ml an O+ leukodepleted RBC transfusion. Immediately after transfusion was completed, there is a short-term deterioration of the general condition. Cyanosis, stiffness, trismus, and bradycardia appear within a few seconds. DAT was negative, bilirubin in the reference range. After transfusion, laboratory, echosonographic examination, neurological examination, EEG and ECG showed normal results. It was concluded that the adverse reaction was probably caused by transfusion. Conclusion: In preterm infants, hypocalcaemia may occur during transfusion due to citrate overload. Children of diabetic mothers, on antibiotic and photo therapy are at higher risk of developing hypocalcemia. Future studies should evaluate incidence rate of adverse transfusion reactions in newborns.

Persistent Aortic Stiffness and Left Ventricular Hypertrophy in Children of Diabetic Mothers

BackgroundFetuses of diabetic mothers develop left ventricular (LV) hypertrophy and are at increased long-term risk of cardiovascular disease. In our previous longitudinal study from midgestation to late infancy we showed persistence of LV hypertrophy and increased aortic stiffness compared with infants of healthy mothers, the latter of which correlated with third trimester maternal hemoglobin A1c. In the present study, we reexamined the same cohort in early childhood to determine if these cardiovascular abnormalities persisted. MethodsHeight, weight, and right arm blood pressure were recorded. A full functional and structural echocardiogram was performed with offline analysis of LV posterior wall and interventricular septal diastolic thickness (IVSd), systolic and diastolic function, and aortic pulse wave velocity. Vascular reactivity was assessed using digital thermal monitoring. Participants also completed a physical activity questionnaire. ResultsTwenty-five children of diabetic mothers (CDMs) and 20 children from healthy pregnancies (mean age, 5.6 ± 1.7 and 5.3 ± 1.3 years, respectively; P = not significant) were assessed. Compared with controls, IVSd z score was increased in CDMs (1.2 ± 0.6 vs 0.5 ± 0.3, respectively; P = 0.006), with one-fifth having a z score of more than +2.0. Aortic pulse wave velocity was increased in CDMs (3.2 ± 0.6 m/s vs 2.2 ± 0.4 m/s; P = 0.001), and correlated with IVSd z score (R2 = 0.81; P = 0.001) and third trimester maternal A1c (R2 = 0.65; P < 0.0001). Body surface area, height, weight, blood pressure, vascular reactivity, and physical activity scores did not differ between groups. Our longitudinal analysis showed that individuals with greater IVSd, and aortic stiffness in utero, early and late infancy also tended to have greater measures in early childhood (P < 0.001 and P < 0.0001, respectively). ConclusionsCDMs show persistently increased interventricular septal thickness and aortic stiffness in early childhood.

Cardiomyopathy and cardiac function in fetuses and newborns of diabetic mothers

ObjectiveTo evaluate cardiac function and structural changes in children of diabetic mothers in the fetal and neonatal period using Doppler-echocardiographic data. MethodA prospective, descriptive observational study conducted in a private and tertiary care service for high-risk pregnant women. It included 48 children of mothers with gestational diabetes mellitus (GDM) considered clinically compensated during pregnancy, with a single fetus and absence of malformations. Myocardial thickness, shortening fraction, left ventricular (LVMPI) and right ventricular (RVMPI) myocardial performance index, and mitral and tricuspid valve E/A ratio were evaluated in 96 echocardiographic exams with Doppler. ResultsThe hypertrophic cardiomyopathy was 29% vs 6% p = 0.006 in the prenatal and postnatal periods respectively. The shortening fraction was 0% vs 6% p = 0.242 in the fetuses and newborns respectively. The myocardial performance index of the right ventricle was 12% vs 54% p ≤ 0.001, and on the left ventricle 27% vs 60% p = 0.001 in the prenatal and postnatal periods respectively. The ratio of mitral valve E/A waves was 6% vs 50% p ≤ 0.001 and the ratio of tricuspid valve E/A waves was 0% vs 27% p ≤ 0.001 in the fetuses and newborns respectively. ConclusionA decrease in the rate of myocardial hypertrophy and changes in cardiac function parameters were observed in the fetal and neonatal periods.

Sex differences in offspring neurodevelopment, cognitive performance and microglia morphology associated with maternal diabetes: Putative targets for insulin therapy

Diabetes during pregnancy has been shown to affect the central nervous system (CNS) of the offspring, resulting in short- and long-term adverse effects. Children of diabetic mothers are more likely to develop cognitive impairment, also having increased susceptibility to psychiatric disorders. Microglia, the immune cells of the CNS, work as sensors of environmental changes, namely metabolic challenges, as early as the intrauterine period. During this period, microglia is actively involved in processes of neurogenesis, synaptic pruning and detection of any environmental alteration that may impact brain development. The remarkable sex dimorphism in neurodevelopment, as well as sex differences in the morphology and immune function of microglia during development, led us to clarify if maternal diabetes affects specific behavioral traits and microglia morphology during infancy in a sex-specific manner. Another important goal of this study was to clarify if insulin, the gold standard treatment of diabetes during gestation, could prevent maternal diabetes-induced behavioral changes, as well as microglia morphology, also considering sex specificities. Other molecular and cellular players potentially involved in the link between changes in metabolism and behavior were also analyzed in the hippocampus, a brain region implicated in cognition and other behavioral outcomes. Diabetes during pregnancy globally delayed female and male offspring development and was associated with impairments in recognition memory, but only in female offspring. In line with these results, at early and late infancy, some molecular and cellular markers were altered in offspring hippocampus in a sex-specific manner. The strict control of glycemia by insulin during pregnancy prevented most of the negative effects induced by uncontrolled hyperglycemia. Notably, insulin administration to diabetic dams may also modulate offspring development in a way that differs from what is observed in physiological conditions, since it promoted the expedited acquisition of developmental milestones and of discrimination ability at memory test, also inducing a hyper-ramification of male and female hippocampal microglia. Importantly, this study highlights the importance of analyzing the impact of maternal diabetes and insulin therapy, taking into account sex differences, since male and female present different vulnerabilities to hyperglycemia in this critical period of life.

Volumetric investigation of the hippocampus in rat offspring due to diabetes in pregnancy–A stereological study

BackgroundThe brain development during the prenatal period is affected by various factors, including the mother's metabolic condition. It has been revealed that diabetes in pregnancy is associated with structural and functional alterations in offspring’s hippocampus. Hippocampus, as a critical region with well-known roles in learning and memory consolidation, is vulnerable to changes in glucose level. This study was designed to investigate the effects of maternal diabetes during the pregnancy period and insulin therapy on the neuronal density and the volume of different subfields of the hippocampus in rat offspring at postnatal day 14 (P14). MethodsWistar female rats were randomly divided into diabetics (STZ-D), diabetes treated with insulin (STZ-INS) group, and controls (CON). The animals in all groups were mated by non-diabetic male rats. Two weeks after birth, male pups from each group were sacrificed. The Cavalieri method was carried out to estimate the total volume, and the numerical density of the neurons in the hippocampus and its sub regions was measured by the optical dissector technique. ResultsBilateral hippocampal volume decreased in the diabetic group, mainly in the CA1, dentate gyrus (DG) and subiculum areas (P ≤ 0.05), when compared to control and insulin-treated diabetic animals. In all hippocampus sub-regions, maternal diabetes resulted in a significant decrease in the number of cells in comparison with two other groups (P ≤ 0.05 each). ConclusionThese data indicate that diabetes during pregnancy has a negative impact on the development of the hippocampus in the rats. These changes in the volume of hippocampal CA1, DG, and subiculum areas might be at the core of underlying neurocognitive and neurobehavioral impairments observed in the children of diabetic mothers.

Maternal Diabetes Mellitus as a Risk Factor for High Blood Pressure in Late Childhood.

Intrauterine fetal conditions can have lifelong cardiovascular effects. The impact of maternal diabetes mellitus on children's cardiovascular profile is not well established. The goal of this study was to explore the association between maternal diabetes mellitus and offspring's blood pressure (BP) ≤10 years of age. Generation XXI is a prospective birth cohort, which enrolled 8301 mother-offspring pairs, including 586 (7.1%) children of diabetic mothers. The associations between maternal diabetes mellitus and BP at 4, 7, and 10 years of age was modeled using linear regression. A mixed-effects model was built to assess differences in BP variation over time. Path analysis was used to quantify effects of potential mediators. Maternal diabetes mellitus was associated with higher BP in offspring at the age of 10 (systolic: β, 1.48; 95% CI, 0.36-2.59; and diastolic: β, 0.86; 95% CI, 0.05-1.71). This association was independent of maternal perinatal characteristics, and it was mediated by child's body mass index and, to a lesser extent, by gestational age, type of birth, and birth weight (indirect effect proportion, 73%). No significant differences in BP were found at 4 and 7 years of age. Longitudinal analysis showed an accelerated systolic BP increase on maternal diabetes mellitus group (β, 1.16; 95% CI, 0.03-2.28). These finding were especially relevant in males, suggesting sex differences in the mechanisms of BP prenatal programing. Our results provide further evidence that maternal diabetes mellitus is associated with high BP late in childhood, demonstrating a significant role of child's body mass in the pathway of this association.

Left ventricular mass in offspring of diabetic mothers: at 5–7 years old

Newborns of mothers with diabetes have increased risk for cardiac left ventricular (LV) hypertrophy. Diabetic pregnancy is also associated with in increased risk for obesity and hypertension, as well as for later cardiovascular morbidity and mortality. This study aimed to examine the connection between being the offspring from a diabetic pregnancy and having hypertension and obesity to the increased risk to have left ventricular mass (LVM) and altered LV geometry in childhood. We conducted a retrospective cohort study on 23 offspring of diabetic mothers and 23 sex- and age-matched control children at the age of 5–7 years. LVM and LV geometry were assessed using M-mode echocardiography and indexed for height2.7. Data analyses were adjusted for birth weight, current overweight/obesity status and blood pressure. Prevalence of increased LVM/height2.7 was higher in children of diabetic mothers, i.e. 43.5 vs. 8.7% in the control group (RR (95% CI) 5.0 (1.2–20.4), p = 0.007). The association between maternal diabetes and increased LVM persisted after adjustment for age, sex, birth weight, current overweight/obesity status and blood pressure, with regression coefficient of (95% CI) 5.7 (1.4–10.1), p = 0.01. Together, maternal diabetes, overweight/obesity status and blood pressure contributed 50% to the increase. Results showed that children of diabetic mothers were more likely to have altered LV geometry (RR (95% CI) 6.0 (1.5–23.9), p < 0.001). Maternal diabetes is a risk factor for increased LVM and altered LV geometry in childhood.

Maternal and paternal family history of diabetes in second-degree relatives and metabolic outcomes at age 5–6 years: The ABCD Study

AimTo investigate whether children with a family history of diabetes (FHD) in second-degree relatives (grandparents, aunts/uncles) are at increased risk of developing obesity and diabetes, and whether the risk differs between maternal or paternal transmission. MethodsIn the multiethnic population-based cohort Amsterdam-Born Children and Their Development (ABCD) Study, body mass index (BMI), waist-to-height ratio (WHR), fat percentage (fat%), fasting glucose and C-peptide in 5- or 6-year-old children with no second-degree FHD (n=2226) were compared with children with maternal-only (n=353), paternal-only (n=281) or both maternal and paternal (n=164) second-degree FHD. Children of diabetic mothers or fathers were excluded. ResultsNone of the children in any of our FHD categories differed in body composition after adjusting for maternal, paternal and childhood lifestyle covariates. However, children with both maternal and paternal second-degree FHD had increased C-peptide levels (0.03nmol, 95% CI: 0.01–0.05) compared with those in the other three study groups. Results were similar when analyses were restricted to only the Dutch children. ConclusionChildren with FHD in second-degree relatives on both maternal and paternal sides already have higher C-peptide levels at an early age. This might be the result of a double burden of a shared obesogenic lifestyle, or of more diverse diabetogenic genes compared to children without FHD or with only FHD in one side of the family. In any case, second-degree FHD could be used as a public-health screening tool to identify children at risk of adverse metabolic outcomes and of possible future disease.

Intrauterine fetal demise with caudal regression syndrome, a case report

Background: The causes of intrauterine fetal demise are varied and not entirely well-understood. Multiple observational studies have shown that both perinatal and infant mortality rates are increased in children of diabetic mothers when compared to those of nondiabetic mothers. Case: We present a case involving a 22-year-old G4P0120 with poorly controlled type 1 diabetes mellitus and a complex medical history including two first trimester fetal losses, and second trimester intrauterine fetal demise who presented during the second trimester for care and was found to have a fetus with ultrasound findings consistent with caudal regression syndrome. When she presented in labor at term intrauterine fetal demise was identified. Discussion: Infants and fetuses of diabetic mothers are at a higher risk for congenital anomalies, one of which is the potentially devastating caudal regression syndrome. However, it appears that this risk may be lowered with strict glycemic control both before and during pregnancy.

Associations of growth patterns and islet autoimmunity in children with increased risk for type 1 diabetes: a functional analysis approach.

Several studies indicate associations between early growth and type 1 diabetes (T1D). However, it remains an open question whether these findings can be translated to typical growth patterns associated with increased risk for T1D-associated islet autoimmunity. We analyzed pooled data from 2236 children followed up in two large prospective German birth cohorts with a genetically increased risk for T1D including 18 564 measurements of height and weight, which were transformed to sex- and age-specific standard deviation scores (SDS). A total of 191 children developed any islet autoantibodies, 101 multiple islet autoantibodies. We applied a model-based clustering technique to derive typical height and body mass index (BMI) growth patterns, stratified for maternal T1D status. These patterns were used to predict islet autoimmunity in logistic regression models, adjusted for potential confounders. Growth patterns were not associated with islet autoimmunity in the whole dataset and in children of diabetic mothers, respectively. In children of non-diabetic mothers ,however, islet autoimmunity was associated with rapidly increasing BMI SDS values until the age of 3 yr [adjusted odds ratio (95% confidence interval): 2.02 (1.03, 3.73) for development of any islet autoantibodies) and with consistently above average height SDS values [odds ratio: 2.21 (1.15, 4.17)]. In contrast, a pattern of high height SDS values at birth followed by a decrease to average values after 3 yr was associated with a reduced rate of islet autoimmunity [odds ratio: 0.16 (0.01, 0.62)]. Early growth patterns may be associated with T1D-related islet autoimmunity risk in children of non-diabetic mothers.

MATERNAL DIABETES MELLITUS AND ITS IMPACT ON CHILD NEURODEVELOPMENT; SYSTEMATIC REVIEW

at present, diabetes has become a global health problem. The consequences that entails, both short and long term, do more studies and knowledge necessary for detection, control and treatment. Moreover, its prevalence is increasing in both the general population and pregnant women. Numerous effects and complications have been reported in infants of diabetic mothers, such as fetal macrosomia, hypoglycemia and increased risk of developing obesity. This condition could have negative effects on the neurological development of the child and could affect his intellectual capacity and increase cognitive impairment. to analyze the studies which have investigated in the relationship between diabetes mellitus during pregnancy and its impact on child neurodevelopment short and long-term. we performed a systematic search and 20 specific articles on the subject selected would be selected following the PRISMA guidelines. in the studies consulted include a large methodological variety in both instruments and cognitive assessment scales, as in the age at which the sample is studied. However, most researchers conclude that maternal diabetes can have consequences for the child, both short and long-term. A higher rate of obesity, impaired glucose tolerance, cardiovascular and metabolic disorders and neurodevelopmental impairment is also described, which increase the neurobehavioral disorders and intellectual disability. most of the studies are agree in describing neurodevelopmental disorders in children of diabetic mothers, both in cognition and in the specific areas related to expressive language, social relations, graphical skills and psychomotor development. Other research has linked maternal diabetes with an increased incidence of autism spectrum disorders such as hyperactivity, attention deficits and schizophrenia.

Functional and Anatomic Consequences of Diabetic Pregnancy on Memory in Ten-Year-Old Children.

Pregnancies complicated by diabetes mellitus impair offspring memory functions during infancy and early childhood. The purpose of this study was to investigate the long-term consequences of such pregnancies on memory and memory-related brain regions in 10-year-old children. Nineteen children of diabetic mothers (CDMs) and 35 children of nondiabetic mothers participated in this 10-year follow-up study. Memory performance was assessed using a continuous recognition memory task during which children made old/new judgments in response to pictures of concrete and abstract objects presented after different lags or delays. In addition, the volume of the hippocampal formation (HF) was measured using high-resolution structural images. At 10 years of age, recognition memory performance of CDMs did not differ from children of nondiabetic mothers. Similarly, the volume of the HF did not differ between groups. However, the size of the HF in CDMs predicted the time those children needed to provide accurate responses in the continuous recognition memory task. CDMs do not show memory impairments by 10 years of age, despite evidence for such impairments early in life. However, subtle differences in underlying neural processes may still be present. These results have important implications for long-term cognitive development of CDMs.

Abstract P252: Effect of Maternal Diabetes on Fetal Programming of Vascular Remodeling Mechanisms in Adult Rats

Modifications of the intra-uterine environment are now recognized as an important cause of fetal stress. Leading to several responses such as loss of structure/function and pre-emptive adaptations to an adverse post-natal environment, and finally to adult diseases. It has been demonstrated that children of diabetic mothers have an increased risk of developing cardiovascular diseases (i.e. hypertension) during adulthood. Blood vessels are able to reorganize their structure in response to physiological alteration of blood flow or pathological stimuli. Constrictive vascular remodeling is currently associated with the occurrence of cardiovascular diseases. Thus, our objective was to study vascular remodeling in case of in utero exposure to maternal diabetes. This is in order to investigate the effect of intra-uterine environment perturbations on vascular fetal programming. We have developed an animal model of rats exposed in utero to moderated maternal hyperglycemia (DMO), which developed an hypertension around 6 months of age. We analyzed structure of elastic and resistance arteries (internal diameter, MCSA, intima-media thickness and remodeling parameters) in absence or presence of established hypertension in male DMO compared to controls (CMO) (at 3 and 18 months of age). Moreover, by in vivo sequential ligation of mesenteric arteries, we have studied vascular remodeling of resistance arteries in response to low (LF), normal (NF) or high flow (HF). In old DMO, we did not observe any vascular remodeling induced by hypertension neither in aorta nor in mesenteric arteries. This could be related to the increase of smooth muscle cell attachments that we observed. Moreover, after 1 or 3 weeks of mesenteric arteries ligation, DMO did not exhibit any constrictive remodeling in LF although expansive remodeling in HF is maintained. Interestingly, we measured an increase of eNOS activity and GP91 in LF arteries of theses animals although transglutaminase-2 protein expression was not modified. Our results demonstrate that in utero exposure to maternal diabetes induce modification of vascular remodeling mechanisms in adulthood. Absence of vascular response could be a pre-emptive adaptation to fetal programmed-hypertension in these animals.

Renal echo-3D and microalbuminuria in children of diabetic mothers: a preliminary study.

Maternal diabetes has assumed epidemic relevance in recent years and animal studies have provided some evidence that it may cause abnormalities in renal development and a reduction in nephron endowment in the offspring; however, human data are lacking. The renal cortex contains ∼95% of the glomeruli and its volume could be taken as a surrogate measure of glomerular number; based on this assumption, we measured renal cortex volume and in addition, microalbuminuria in a homogeneous sample of 42 children of diabetic (pregestational, n = 13, and gestational, n = 29) mothers, compared with 21 healthy children born of non-diabetic mothers. The offspring of diabetic mothers showed a significant reduction of renal cortex volume and higher albumin excretion compared with controls, possibly attributable to a reduction in the number of nephrons and the difference was statistically significant (P < 0.001). Although further studies on a larger sample are necessary, our preliminary findings suggest that maternal diabetes may affect renal development with sequelae later in life, requiring closer monitoring and follow-up. Furthermore, the importance of strict maternal diabetes management and control must be emphasized.

Is maternal diabetes a risk factor for childhood obesity?

Objective: Our objective is to determine if there is a relationship between diabetes during pregnancy and childhood obesity, in our inner-city, African–American population. Methods: Pertinent child, neonatal and maternal pregnancy and delivery data were collected from mothers of children age 2–5 years old. Outcome variable definition was based on children’s body mass index (BMI) subgroups; independent variable definition on birthweight subgroups based on customized growth percentiles. Covariates included pre and postnatal factors. Those covariates marginally related to diabetes (p < 0.2) by bivariate analyses, were allowed to compete in logistic regression, with p < 0.05 significant. Results: Four hundred and ninety-three patients were enrolled, of which 35 (7.1%) had diabetes during pregnancy. Children of diabetic mothers were more likely to be obese at age 2–5 years than those of non-diabetics (p = 0.004). Five of 20 covariates had p < 0.2 in bivariate setting. Following stepwise logistic regression, diabetes and maternal prepregnancy BMI were significant determinants of childhood obesity. When large-for-gestational age (LGA) was added into the model, diabetes was no longer significant (p = 0.105); only LGA (p = 0.008) and maternal prepregnancy BMI (p = 0.032) were significantly associated with childhood obesity. Conclusions: In our inner-city, primarily African–American population, diabetes in pregnancy is significantly related to childhood obesity at age 2–5 years. Well-controlled diabetes during pregnancy that avoids macrosomia may lead to prevention of future childhood obesity as well.

Obesity in the pregnant diabetic population and delivery outcomes

IntroductionDiabetes is the most common pre-existing medical condition in pregnancy in the UK. The global obesity epidemic has led to an increase in the incidence of Type 2 Diabetes in...

Cortical Evoked Potentials in Children of Diabetic Mothers

Type 1 diabetic mothers' infants show a delay of visual evoked potential (VEP) significantly related to some parameters of poor metabolic control during pregnancy. In the present paper we analyzed the characteristics of VEPs and somatosensory evoked potentials (SEPs) recorded in 16 three-year-old type 1 diabetic mothers' children (DMC). Compared with controls (23 nondiabetic mothers' healthy matched children), DMC showed significantly delayed mean latency of VEP (P2) and SEP (P22). In 3 cases (19%), we found pathological responses (+3 SD from the mean value of controls) of VEPs and SEPs. At the age of 3 years, the offspring of type 1 diabetic mothers showed delay of cortical evoked responses in both visual and somatosensory systems.