In humans, maternal obesity has been linked to greater placental mitochondrial content and lipotoxicity which may contribute to altered offspring outcomes. Thus, interventions to improve maternal health during pregnancy are needed. In a RCT, we compared placental mitochondrial respiration of obese women who consumed probiotics (PR, B. Lactis bb 12® and L. rhamnosus GG, n=12) vs. placebo (PL, n=7) from gestation week 12 until delivery.


Mitochondrial respiration was measured using high resolution respirometry (HRR). A protocol that provides information on the fatty oxidation pathway (FAO) was applied: 1) Octanoylcarnitine + Malate (OctM). 2) Complex (C) I-linked substrates (pyruvate and glutamate, FAO&CI). 3) CII-linked substrate (Succinate, FAO&CI&CII). 4) Glycerophosphate (Gp, FAO&CI&CII&Gp): 5) FCCP obtained electron transport capacity (ET, uncoupled ET state). 6) Rotenone and antimycin-A measured residual oxygen consumption (ROX). Data were normalized per mg of tissue, and with flux control ratios (FCR) to account for potential differences in mitochondrial content. Data presented as mean±SEM. HRR data presented in pmol O2•s-1•mg-1.


BMI (PR=36±1 vs. PL=36±2 kg/m2) at enrollment, and gestational age at delivery (PR=39± 0.4 vs. PL=39± 0.3 wk) were comparable between groups. FAO (PR=3.4±0.6 vs. PL=5.3±0.6, p=0.062); FAO&CI (PR=5.0±0.4 vs. PL=8.0±0.9, p=0.009); FAO&CI&CII (PR=11.9±1.1 vs. PL=17.5±1.4, p=0.009); FAO&CI&CII&Gp (PR=13.9±1.3 vs. PL=19.5±1.7, p=0.025); ET (PR=22.8±2.1 vs. PL=29.7±2.2, p=0.043); ROX (PR=1.8±0.8 vs. PL=6.4±5.7, p=0.023) decreased with PR supplementation. When FCR were created no differences were seen between groups suggesting a mediation via altered mitochondrial content.


Placental mitochondrial respiration of obese women decreases with probiotic supplementation during pregnancy potentially through a decrease in placenta mitochondrial content. The mechanisms involved will be further investigated. NIH-P20GM109096, USDA-ARS 6026-51000-010-05S