Jacinta Byrne

Prevalence of physical activity among healthy pregnant women in Ireland.

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Leptin, fetal growth and insulin resistance in non-diabetic pregnancies.

BACKGROUND Interrogation of the association between leptin, insulin resistance and fetal growth may provide a biological link for the fetal programming of later metabolic health. AIMS Our aim was to clarify the relationship between maternal and fetal leptin, insulin resistance and fetal growth. STUDY DESIGN Maternal leptin, glucose and insulin were measured in early pregnancy and at 28weeks and the HOMA index calculated. At 34weeks, ultrasound scan assessed fetal weight and adiposity (abdominal wall width). At delivery birthweight was recorded and cord blood analyzed for fetal c-peptide and leptin. Analysis was performed using a multivariate linear regression model. SUBJECTS 574 non-diabetic pregnant women. OUTCOME MEASURES Fetal growth and maternal and fetal insulin resistance. RESULTS On multivariate analysis a relationship was identified between maternal and fetal leptin concentrations at each time point and maternal body mass index. Maternal leptin was related to insulin resistance in early pregnancy (β=0.15, p=0.02) and at 28week gestation (β=0.27, p<0.001). Fetal insulin resistance correlated with maternal leptin in early pregnancy (β=0.17, p=0.004); at 28weeks (β=0.12, p=0.05), and with leptin in cord blood (r=0.28, p<0.001). Fetal weight at 34weeks was related to maternal leptin in early pregnancy (β=0.16, p=0.02). Both maternal and fetal leptin correlated with infant size at birth (β=0.12, p=0.07 in early pregnancy, β=0.21, p=0.004 in cord blood), independent of all other outcome measures. CONCLUSION Our findings have confirmed that in a non-diabetic cohort there is a link between maternal and fetal leptin and insulin resistance. We also established a link between maternal leptin in early pregnancy and both fetal and neonatal size. These results add to the growing body of evidence suggesting a role for leptin in the fetal programming of childhood obesity and metabolic dysfunction.

Impact of maternal diet on neonatal anthropometry: a randomized controlled trial

Large for gestational age infants are at increased risk of childhood obesity and maternal nutrition impacts birthweight. The aim of this study was to assess the impact of a maternal low glycaemic index (GI) diet on neonatal anthropometry.

Insufficient vitamin D intakes among pregnant women

Vitamin D has an important role in pregnancy in promoting fetal skeletal health. Maternal dietary intake is a key factor influencing both maternal and fetal status. There are limited data available on food groups contributing to vitamin D intake in pregnancy. The aim of this study was to determine dietary intakes of vitamin D throughout pregnancy in 64 women and to determine the main food groups contributing to vitamin D intake. Results showed that median dietary intakes of vitamin D ranged from 1.9–2.1 μg/d during pregnancy, and were 80% below the current recommendation. The principal food groups contributing to vitamin D intake were meat, egg and breakfast cereal groups. Oily fish, the best dietary source of vitamin D, was consumed by <25% of women. These data call for more education; they question the role of vitamin D supplementation and highlight the contribution of other food groups more frequently consumed, namely, breakfast cereals, meat and eggs.

Maternal Nutrition and Glycaemic Index during Pregnancy Impacts on Offspring Adiposity at 6 Months of Age—Analysis from the ROLO Randomised Controlled Trial

Childhood obesity is associated with increased risk of adult obesity and metabolic disease. Diet and lifestyle in pregnancy influence fetal programming; however the influence of specific dietary components, including low glycaemic index (GI), remains complex. We examined the effect of a maternal low GI dietary intervention on offspring adiposity at 6 months and explored the association between diet and lifestyle factors in pregnancy and infant body composition at 6 months. 280 6-month old infant and mother pairs from the control (n = 142) and intervention group (n = 138), who received low GI dietary advice in pregnancy, in the ROLO study were analysed. Questionnaires (food diaries and lifestyle) were completed during pregnancy, followed by maternal lifestyle and infant feeding questionnaires at 6 months postpartum. Maternal anthropometry was measured throughout pregnancy and at 6 months post-delivery, along with infant anthropometry. No difference was found in 6 months infant adiposity between control and intervention groups. Maternal trimester three GI, trimester two saturated fats and trimester one and three sodium intake were positively associated with offspring adiposity, while trimester two and three vitamin C intake was negatively associated. In conclusion associations were observed between maternal dietary intake and GI during pregnancy and offspring adiposity at 6 months of age.

The association between TNF-α and insulin resistance in euglycemic women

Chronic low levels of inflammation have links to obesity, diabetes and insulin resistance. We sought to assess the relationship between cytokine tumor necrosis factor (TNF-α) and insulin resistance in a healthy, euglycemic population. This is a prospective study of 574 non-diabetic mother and infant pairs. Maternal body mass index (BMI), TNF-α, glucose and insulin were measured in early pregnancy and at 28 weeks. Insulin resistance was calculated by HOMA index. At delivery birthweight was recorded and cord blood analysed for fetal C-peptide and TNF-α. In a multivariate model, maternal TNF-α in early pregnancy was predicted by maternal insulin resistance at the same time-point, (β=0.54, p<0.01), and maternal TNF-α at 28 weeks was predicted by maternal insulin resistance in early pregnancy (β=0.24, p<0.01) and at 28 weeks (β=0.39, p<0.01). These results, in a large cohort of healthy, non-diabetic women have shown that insulin resistance, even at levels below those diagnostic of gestational diabetes, is associated with maternal and fetal inflammatory response. These findings have important implications for defining the pathways of fetal programming of later metabolic syndrome and childhood obesity.