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Updated: Nov 8, 2025

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Saturated free fatty acids induce placental trophoblast lipoapoptosis

Sathish Kumar Natarajan1, Taylor Bruett1, Philma Glora Muthuraj1

  • 1Department of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, NE, United States of America.

Plos One
|April 22, 2021
PubMed

Insights

Maternal obesity increases free fatty acids (FFAs), causing placental cell death. Monounsaturated fatty acids protect against this damage, offering a potential therapeutic avenue for pregnancy complications.

Area of Science:

  • Obstetrics and Gynecology
  • Cell Biology
  • Metabolic Disorders

Background:

  • Maternal obesity is linked to adverse pregnancy outcomes, including gestational diabetes and preeclampsia.
  • Increased circulating free fatty acids (FFAs) in obesity can cause cell death in organs like the liver and pancreas.
  • The impact of elevated FFAs on placental cells during pregnancy is not well understood.

Purpose of the Study:

  • To investigate if saturated FFAs induce apoptosis in placental trophoblast cells.
  • To determine if monounsaturated fatty acids can protect against FFA-induced trophoblast apoptosis.
  • To utilize an in vitro cell culture model for these investigations.

Main Methods:

  • Assessed apoptosis using DAPI staining for nuclear morphology and caspase 3/7 activity assays.
  • Utilized western blot analysis to examine cleaved PARP and cleaved caspase 3.
  • Employed JEG-3 and JAR trophoblast cell lines for in vitro experiments.

Main Results:

  • Saturated FFAs (palmitate and stearate) significantly increased trophoblast lipoapoptosis in a dose-dependent manner.
  • Monounsaturated fatty acids (palmitoleate and oleate) effectively mitigated FFA-induced trophoblast lipoapoptosis.
  • Observed increased apoptotic nuclear changes and caspase 3/7 activity upon saturated FFA treatment.

Conclusions:

  • Saturated FFAs induce lipoapoptosis in placental trophoblast cells.
  • Monounsaturated fatty acids demonstrate a protective effect against FFA-induced trophoblast lipoapoptosis.
  • These findings highlight potential mechanisms underlying placental dysfunction in maternal obesity.
Abstract

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