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Updated: Apr 21, 2026

The 4-vessel Sampling Approach to Integrative Studies of Human Placental Physiology In Vivo
Published on: August 2, 2017
Placental growth response to maternal insulin in early pregnancy
Perrie O'Tierney-Ginn1, Larraine Presley, Stephen Myers
1Center for Reproductive Health (P.O.-G., L.P., S.M., P.C.), MetroHealth Medical Center, Cleveland, Ohio 44109; and Department of Reproductive Biology (P.O.-G., S.M., P.C.), Case Western Reserve University, Cleveland, Ohio 44106.
Context:
The sensitivity of the placenta to maternal insulin remains controversial. Early pregnancy may be a time of increased placental sensitivity to maternal insulin because insulin receptors are abundant on the syncytiotrophoblast in the first trimester but are far fewer at term.
Hypothesis:
Maternal insulin secretory response in early, but not late, pregnancy is positively associated with placental growth.
Design:
This is a secondary analysis of a cohort of women (n = 40) recruited before pregnancy.
Outcome Measures:
An iv glucose tolerance test was administered before pregnancy and in early (12-14 weeks) and late (34-36 weeks) pregnancy. Placental volume throughout gestation (in a subset of women via 3-dimensional ultrasound) and weight at birth were recorded.
Results:
Total insulin secretory response in early pregnancy was positively associated with placental volume in early pregnancy (R = 0.79, P = 0.04) and placental weight at term (R = 0.42, P = 0.007). Insulin secretory response before and in late pregnancy was not significantly associated with placental growth. Although neonatal fat mass was strongly correlated with placental weight at term (R = 0.449, P = 0.0003), maternal insulin secretory response was related to neonatal fat mass only at birth in male offspring (R = 0.59, P = 0.008).
Conclusions:
Maternal insulin secretory response in early pregnancy was strongly related to placental weight at birth. Thus, in early pregnancy, increased maternal insulin response as seen in obesity and gestational diabetes mellitus may be a key influence on placental growth, possibly due to the enhanced presence of placental insulin receptors on the maternal villous membrane early in gestation.
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