Objective: Can gestational weight gain in obese women be restricted by 10-h dietary consultations and does this restriction impact the pregnancy-induced changes in glucose metabolism? Design: A randomized controlled trial with or without restriction of gestational weight gain to 6-7 kg by ten 1-h dietary consultations. Subjects: Fifty nondiabetic nonsmoking Caucasian obese pregnant women were randomized into intervention group (n ¼ 23, 2874 years, prepregnant body mass index (BMI) 3574 kg m À2 ) or control group (n ¼ 27, 3075 years, prepregnant BMI 3573 kg m À2 ). Measurements: The weight development was measured at inclusion (15 weeks), at 27 weeks, and 36 weeks of gestation. The dietary intakes were reported in the respective weeks by three 7-day weighed food records and blood samples for analyses of fasting s-insulin, s-leptin, b-glucose, and 2-h b-glucose after an oral glucose tolerance test were collected. Results: The women in the intervention group successfully limited their energy intake, and restricted the gestational weight gain to 6.6 kg vs a gain of 13.3 kg in the control group (P ¼ 0.002, 95% confidence interval (CI): 2.6-10.8 kg). Both s-insulin and s-leptin were reduced by 20% in the intervention group compared to the control group at week 27, mean difference: À16 pmol l À1 (P ¼ 0.04, 95% CI: À32 to À1) for insulin and À23 ng ml À1 (P ¼ 0.004, 95% CI: À39 to À8) for leptin. At 36 weeks of gestation, the s-insulin was further reduced by 23%, À25 pmol l À1 (À47 to À4, P ¼ 0.022) and the fasting b-glucose were reduced by 8% compared with the control group (À0.3 mmol l À1 , À0.6 to À0.0, P ¼ 0.03). Conclusions: Restriction of gestational weight gain in obese women is achievable and reduces the deterioration in the glucose metabolism.

The aim of the study was 1) to evaluate the association of maternal serum levels of placental GH and IGF-I with fetal growth, and 2) to establish reference data for placental GH, IGF-I, and IGF-binding protein-3 (IGFBP-3) in normal pregnancies based on longitudinal measurements. A prospective longitudinal study of 89 normal pregnant women was conducted. The women had, on the average, seven blood samples taken and three ultrasound examinations performed. All had normal umbilical artery pulsatility indexes during pregnancy and gave birth to singletons between 37 and 42 wk gestation with birth weights above -2 SD. Placental GH levels were detectable in all samples from as early as 5 wk gestation and increased significantly throughout pregnancy to approximately 37 wk when peak levels of 22 ng/ml (range, 4.64-69.22 ng/ml) were reached. Subsequently, placental GH levels decreased until birth. The change in placental GH during 24.5-37.5 wk gestation was positively associated with fetal growth rate (P = 0.027) and birth weight (P = 0.027). Gestational age at peak placental GH values (P = 0.007) was associated with pregnancy length. A positive association between the change in placental GH and the change in IGF-I levels throughout gestation was found in a multivariate analysis (r(2) = 0.42; P < 0.001). There was no association between placental GH and IGFBP-3 levels. The change in IGF-I throughout gestation (P = 0.039), but not placental GH, was significantly positively associated with placental weight at birth. We found a significant association between placental GH and fetal growth. In addition, we found a highly significant association between the increase in placental GH and the increase in IGF-I. The gestational age at peak placental GH levels was associated with pregnancy length.