Anthropometry, Glucose Tolerance, and Insulin Concentrations in Indian Children

Abstract

OBJECTIVE -The purpose of this study was to test the hypothesis that the environment experienced by fetuses of mothers with gestational diabetes mellitus (GDM) and mothers with higher glucose concentrations that are in the normal range causes increased adiposity and altered glucose/insulin metabolism in childhood.RESEARCH DESIGN AND METHODS -Children (n ϭ 630) whose mothers were tested for glucose tolerance during pregnancy had detailed anthropometry performed at birth and annually thereafter. At 5 years, plasma glucose and insulin concentrations were measured in the children (2-h oral glucose tolerance test) and their fathers (fasting samples only).RESULTS -Newborns of diabetic mothers (n ϭ 41) were larger in all body measurements than control newborns (babies with nondiabetic parents). At 1 year, these differences had diminished and were not statistically significant. At 5 years, female offspring of diabetic mothers had larger subscapular and triceps skinfold thicknesses (P ϭ 0.01) and higher 30-and 120-min insulin concentrations (P Ͻ 0.05) than control children. Offspring of diabetic fathers (n ϭ 41) were lighter at birth than control children (P Ͻ 0.001); they showed no differences in anthropometry at 5 years. In control children, skinfold thickness and 30-min insulin concentrations were positively related to maternal insulin area under the curve, and skinfold thicknesses were related to paternal fasting insulin concentrations independently of the parents' skinfold thickness and socioeconomic status.CONCLUSIONS -Maternal GDM is associated with adiposity and higher glucose and insulin concentrations in female offspring at 5 years. The absence of similar associations in offspring of diabetic fathers suggests a programming effect in the diabetic intrauterine environment. More research is needed to determine whether higher maternal glucose concentrations in the nondiabetic range have similar effects. Diabetes Care 28:2919 -2925, 2005T he prevalence of type 2 diabetes is escalating in developing countries undergoing the "epidemiologic transition." India is predicted to have 79 million people with type 2 diabetes by the year 2030 (32 million in 2000) (1). Studies in western populations, predominantly among the Pima Indian communities of North America, have shown that individuals whose mothers were diabetic when they were in utero have an increased risk of early obesity and impaired glucose tolerance (IGT) and type 2 diabetes in adult life (2-4). The risk is increased compared with offspring of diabetic fathers and siblings born before the onset of maternal diabetes (3,5), suggesting that it results from the fetal environment in gestational diabetes mellitus (GDM) rather than from genes. Even in nondiabetic pregnancies, variations within the normal range of maternal fasting glucose concentrations are associated with altered neonatal adiposity (6). It is not known whether this is associated with changes in later body size and glucose/insulin concentrations in the offspring.There are few data from India on the preval...

Early manifestation of cardiovascular disease risk factors in offspring of mothers with previous history of gestational diabetes mellitus

“…Numerous previous studies have indicated that maternal diabetes during pregnancy has both short- and long-term adverse effects on offspring [10][11][12][13][14][15]. Metzger and co-workers [26] reported that the frequency of IGT was increased in the adolescent offspring of diabetic mothers and established the hypothesis that ''diabetes begets diabetes'', indicating that the intrauterine environment and the altered glucose regulation in the second and third trimesters absolutely influenced the short-and long-term health of the foetus.…”

“…The frequent occurrence of perinatal morbidities such as macrosomia, injuries of the brachial plexus, neonatal hypoglycaemia, and foetal distress in offspring also results from glucose intolerance during gestation [7]. Furthermore, a number of epidemiological studies have demonstrated that altered glucose metabolism in mothers during pregnancy has both short-and long-term adverse effects on their offspring [10][11][12][13][14][15]. Pedersen and Freinkel established the theory of fuel-mediated teratogenesis, in which the intrauterine environment is influenced by excessive maternal fuels, which may have short-and long-term adverse effects on offspring [16,17].…”

Relationships of maternal and paternal birthweights to features of the metabolic syndrome in adult offspring: an inter-generational study in South India

“…These have generally examined disease outcomes in men and/or women in relation to the birthweight of their children. Diabetes in fathers, for example, is associated with lower offspring birthweight [5][6][7][8][9]. The opposite is true for diabetes in mothers, because gestational diabetes causes fetal macrosomia [10,11].…”

Foetal Programming in a Diabetic Pregnancy: Long-Term Implications for the Offspring

“…The Parthenon Study showed for the first time that maternal diabetes programmes neuroendocrine stress responses in the offspring, suggesting that this may be one of the pathways for their greater cardiovascular risk 47 . Even in the offspring of non-diabetic parents, both maternal and paternal insulin concentrations were positively associated with offspring adiposity and insulin resistance 45 . Thus in India, widespread maternal under nutrition with specific micronutrient deficiencies as well as high rates of gestational hyperglycaemia may programme offspring cardiometabolic disease risk, suggesting a dual teratogenesis 48 .…”

“…The Parthenon study showed that, as expected, neonates of GDM mothers were heavier, longer and more adipose than control babies (offspring of non-GDM mother and non-diabetic father) 45 . There was a clustering of cardiovascular risk markers, including adiposity, higher glucose and insulin concentrations, insulin resistance (based on homeostasis model assessment for insulin resistance; HOMA-IR) and blood pressure in ODM during childhood and adolescence (Figure 2) 45-47 .…”