Objective: It remains uncertain whether leptin and adiponectin levels are correlated in maternal vs. fetal circulations. Little is known about whether leptin and adiponectin affect insulin sensitivity during fetal life.Design and Methods: In a prospective singleton pregnancy cohort (n = 248), we investigated leptin and adiponectin concentrations in maternal (at 24‐28 and 32‐35 weeks of gestation) and fetal circulations, and their associations with fetal insulin sensitivity (glucose/insulin ratio, proinsulin level).Results: Comparing concentrations in cord vs. maternal blood, leptin levels were 50% lower, but adiponectin levels more than doubled. Adjusting for gestational age at blood sampling, consistent and similar positive correlations (correlation coefficients: 0.31‐0.34, all P < 0.0001) were observed in leptin or adiponectin levels in maternal (at 24‐28 or 32‐25 weeks of gestation) vs. fetal circulations. For each SD increase in maternal plasma concentration at 24‐28 weeks, cord plasma concentration increased by 12.7 (95% confidence interval 6.8‐18.5) ng/ml for leptin, and 2.9 (1.8‐4.0) µg/ml for adiponectin, respectively (adjusted P < 0.0001). Fetal insulin sensitivity was negatively associated with cord blood leptin (each SD increase was associated with a 5.4 (2.1‐8.7) mg/dl/µU/ml reduction in cord plasma glucose/insulin ratio, and a 5.6 (3.9, 7.4) pmol/l increase in proinsulin level, all adjusted P < 0.01) but not adiponectin (P > 0.4) levels). Similar associations were observed in nondiabetic full‐term pregnancies (n = 211).Conclusions: The results consistently suggest a maternal impact on fetal leptin and adiponectin levels, which may be an early life pathway in maternal‐fetal transmission of the propensity to obesity and insulin resistance.

Context: It remains uncertain whether maternal IGF-I is associated with fetal growth. Little is known about the role of maternal IGF-II in fetal growth and whether IGF-I or IGF-II is implicated in fetal hypertrophy in gestational diabetes. Objective: The objective of the study was to assess maternal and fetal IGF-I and IGF-II levels in association with fetal growth and gestational diabetes. Study Design, Population, and Outcomes: A singleton pregnancy cohort study (n = 307). The primary outcome was birth weight. Results: Maternal plasma concentrations increased by an average of 55.4% for IGF-I and 11.8% for IGF-II between 24–28 and 32–35 weeks of gestation. The maternal IGF-I but not IGF-II level was correlated with birth weight and placental weight. Adjusting for maternal and infant characteristics, each sd increase in maternal IGF-I level at 24–28 weeks was associated with a 75-g (95% confidence intervals 29–120) increase in birth weight, a 20-g (7–33) increase in placental weight, and a 1.91-fold (1.28–2.86) higher odds of macrosomia (birth weight > 90th percentile). Similar associations were observed for the maternal IGF-I level at 32–35 weeks. Maternal and fetal IGF-I (but not IGF-II) levels were significantly higher in gestational diabetic than in nondiabetic pregnancies. The significantly higher birth weight z scores in diabetic pregnancies disappeared after adjusting for maternal and fetal IGF-I levels alone. Conclusions: Higher maternal IGF-I (but not IGF-II) levels at mid- and late gestation may indicate greater placental and fetal growth. IGF-I (but not IGF-II) may be implicated in fetal hypertrophy in gestational diabetes.

Famine provides quasi-experimental conditions for testing the hypothesis of “programming” health effects by poor nutrition in early life. It remains uncertain whether early life exposure to famine increases the risk of hypertension in adulthood. There is a lack of data on the relative impact of exposure to famine during fetal development versus infancy (<2 years postnatal). We sought to assess the impact of exposure to the 1959–1961 Chinese Great Famine (the largest in human history) during fetal development and infancy on the risks of hypertension, short stature and obesity in adulthood. We conducted a retrospective cohort study of 12,065 adults (46–53 years of age) born 1957–1964 in the Zhongshan and Nanhai municipalities of Guangdong province, China. Adjusting for socio-demographic and lifestyle characteristics, as compared to subjects who were unexposed to famine, the risk of hypertension was not significantly elevated in subjects exposed to famine during fetal development only overall, but was 1.36-fold higher in those exposed during the first trimester of pregnancy only [adjusted odds ratio (OR) 1.36 (95% confidence intervals 1.03–1.79)], 1.83-fold higher in those exposed during infancy only [adjusted OR 1.83 (1.61–2.08)], and 1.31-fold higher in those exposed during both fetal development and infancy [adjusted OR 1.31 (1.14–1.51)]. Exposure to famine during infancy increased the risk of short stature. Early life exposure to famine did not increase the risk of obesity. Exposure to the Chinese Great Famine during the first trimester of pregnancy only, or during infancy only, or during both fetal development and infancy increased the risk of hypertension in adulthood, suggesting an important role of changes in exposure to famine during fetal development and from prenatal to early postnatal life in developmental “programming” cardiovascular disease risk.

Background. Preeclampsia is a serious pregnancy complication. Gestational hypertension is a common first clinical presentation of preeclampsia. Little is known

Objective To assess the associations of gestational weight gain (GWG) in early and late pregnancy with subsequent risks of adverse pregnancy outcomes in Chinese women. Design Prospective cohort study. Setting Shanghai, China. Participants We studied 2630 nulliparous singleton pregnant women with complete data on weight gain in early (≤17 weeks of gestation) and late (>17 weeks) pregnancy in the Shanghai Birth Cohort. Methods GWG was standardised into z-scores by gestational age and categorised as low (z-score <−1), normal (−1 to +1) and high (>1). The adjusted relative risks (aRRs) and 95%CIs were estimated through log-binomial regression models. Interaction effects between GWG and some other adjustment factors were tested, further stratified analyses were performed separately where interaction terms were significant. Outcome measures Adverse maternal and neonatal outcomes. Results Independent from GWG in late pregnancy, higher GWG in early pregnancy was associated with higher risks of gestational diabetes mellitus (aRR: 1.66; 95% CI: 1.11 to 2.48), caesarean section (aRR: 1.21; 95% CI: 1.05 to 1.39) and prolonged hospitalisation (aRR: 1.56; 95% CI: 1.03 to 2.38). Higher GWG in late pregnancy was independently associated with higher risks of caesarean section (aRR: 1.24; 95% CI: 1.09 to 1.41), large for gestational age (aRR: 2.01; 95% CI: 1.50 to 2.7) and macrosomia (aRR: 1.90; 95% CI: 1.30 to 2.78). In addition, the risk of gestational hypertension increased significantly with increased total GWG (aRR: 1.78; 95% CI: 1.14 to 2.76). The effects of GWG in late pregnancy on maternal and neonatal outcomes were significantly different between the women bearing a female and the women bearing male fetus. Conclusion The GWG associations with adverse pregnancy outcomes differ at early and late pregnancy, and there may be effect modification by fetal sex in the association of GWG in late pregnancy with some pregnancy outcomes.

Arachidonic acid (AA; C20∶4 n-6) and docosahexaenoic acid (DHA; C22∶6 n-3) are important long-chain polyunsaturated fatty acids (LC-PUFA) in maintaining pancreatic beta-cell structure and function. Newborns of gestational diabetic mothers are more susceptible to the development of type 2 diabetes in adulthood. It is not known whether low circulating AA or DHA is involved in perinatally “programming” this susceptibility. This study aimed to assess whether circulating concentrations of AA, DHA and other fatty acids are associated with fetal insulin sensitivity or beta-cell function, and whether low circulating concentrations of AA or DHA are involved in compromised fetal insulin sensitivity in gestational diabetic pregnancies. In a prospective singleton pregnancy cohort, maternal (32-35 weeks gestation) and cord plasma fatty acids were assessed in relation to surrogate indicators of fetal insulin sensitivity (cord plasma glucose-to-insulin ratio, proinsulin concentration) and beta-cell function (proinsulin-to-insulin ratio) in 108 mother-newborn pairs. Cord plasma DHA levels (in percentage of total fatty acids) were lower comparing newborns of gestational diabetic (n = 24) vs. non-diabetic pregnancies (2.9% vs. 3.5%, P = 0.01). Adjusting for gestational age at blood sampling, lower cord plasma DHA levels were associated with lower fetal insulin sensitivity (lower glucose-to-insulin ratio, r = 0.20, P = 0.036; higher proinsulin concentration, r = −0.37, P <0.0001). The associations remained after adjustment for maternal and newborn characteristics. Cord plasma saturated fatty acids C18∶0 and C20∶0 were negatively correlated with fetal insulin sensitivity, but their levels were not different between gestational diabetic and non-diabetic pregnancies. Cord plasma AA levels were not correlated with fetal insulin sensitivity. Low circulating DHA levels are associated with compromised fetal insulin sensitivity, and may be involved in perinatally “programming” the susceptibility to type 2 diabetes in the offspring of gestational diabetic mothers.