OBJECTIVE -To assess the association of fetal hormones with placental growth and fetal weight-to-placental weight ratio index (FPI) in pregnancies complicated by maternal diabetes.RESEARCH DESIGN AND METHODS -We conducted a prospective study using umbilical venous blood samples taken at birth from 122 offspring of mothers with type 1 diabetes (OT1D) and 46 control subjects.RESULTS -Placental weight (P ϭ 0.009) and gestation-adjusted birth weight (P Ͻ 0.001) were increased in OT1D, but FPI was unaltered (P ϭ 0.33). Placental weight correlated with birth weight (P Ͻ 0.001) and cord leptin (P Ͻ 0.001) in control subjects and OT1D, with further relationships with cord insulin, IGF-1, IGF-binding protein-3 (IGFBP-3), and triceps and subscapular thickness in OT1D. FPI was associated with adiponectin in both groups, even after adjustment for confounders.CONCLUSIONS -Placental and fetal growth show a parallel increase in mothers with type 1 diabetes. The possible role of adiponectin in matching of fetal and placental growth merits further study.
Diabetes Care 31:1123-1125, 2008P lacental weight is strongly associated with birth weight, with experimental and epidemiological studies demonstrating associations of reduced fetal weight-to-placental weight ratio index (FPI) with later hypertension, glucose intolerance, and coronary heart disease, suggesting in utero programming of adult disease (1). Fetal adiponectin, an adipokine with insulin-sensitizing and antiinflammatory effects, has been identified as the first biomarker associated with FPI (2). In this study, we examined FPI and its relation to hormonal indexes, in particular those of insulin and adiponectin, in offspring of mothers with type 1 diabetes (OT1D), a group observed to exhibit reduced FPI (3) and adiponectin (4) and to be subject to in utero programming of glucose intolerance (5).
RESEARCH DESIGN ANDMETHODS -A comprehensive description of prospective recruitment and exclusion criteria are available in previous publications (4,6). A total of 122 OT1D and 46 control subjects were available for analysis. FPI (birth weight [grams] divided by placental weight [grams]) was calculated for each delivery. Maternal A1C and cord plasma insulin, leptin, IGF-1, IGFBP-3, adiponectin, C-reactive protein (CRP), and intracellular adhesion molecule-1 were assayed centrally (4,6). Hemoglobin and hematocrit (available in 32 control subjects and 81 OT1D) were measured locally by routine clinical hematological analyzers. A1C was included when assessed between weeks 26 and 34 of pregnancy (available in 90 OT1D).Results are presented as mean Ϯ SD or unadjusted median (interquartile range). Pearson correlations, general linear models, and stepwise logistic regression (P Յ 0.15 for inclusion of predictors) on log-transformed variables were used to assess relationships.RESULTS -Mean Ϯ SD birth weight (control subjects 3,553 Ϯ 520 g, OT1D 3,778 Ϯ 701 g; P Ͻ 0.001) and placental weight (control subjects 627 g [551-700], OT1D 700 g [600 -800]; P Ͻ 0.001) were increased in OT1D, with no ...