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Gestational Diabetes-like Fuels Impair Mitochondrial Function and Long-Chain Fatty Acid Uptake in Human Trophoblasts

Kyle M Siemers1, Lisa A Joss-Moore2, Michelle L Baack3,4

  • 1Sanford School of Medicine, University of South Dakota, 414 E. Clark Street, Vermillion, SD 57069, USA.

International Journal of Molecular Sciences
|November 9, 2024
PubMed

Insights

Gestational diabetes mellitus (GDM) impairs placental fatty acid (FA) uptake and lipid droplet storage, especially with combined high glucose and lipids. This contributes to fetal long-chain polyunsaturated fatty acid (LCPUFA) deficiency and adverse outcomes.

Area of Science:

  • Reproductive Biology
  • Maternal-Fetal Medicine
  • Cellular Metabolism

Background:

  • Gestational diabetes mellitus (GDM) leads to maternal hyperglycemia and hyperlipidemia.
  • Infants exposed to GDM face risks of essential long-chain polyunsaturated fatty acid (LCPUFA) deficiency.
  • Mechanisms linking diabetic fuels to placental fatty acid (FA) transport and lipid droplet dynamics are unclear.

Purpose of the Study:

  • To investigate how high glucose and high lipid conditions, individually and combined, affect trophoblast function.
  • To analyze the impact on trophoblast growth, viability, mitochondrial function, FA uptake, and lipid droplet partitioning.
  • To elucidate how GDM-associated metabolic changes disrupt placental lipid handling.

Main Methods:

  • Utilized BeWo and primary isolated cytotrophoblasts (CTBs) exposed to varying glucose and lipid concentrations.
  • Assessed trophoblast growth, viability, and apoptosis.
  • Measured mitochondrial bioenergetics and BODIPY-labeled fatty acid (FA) uptake, including specific chain lengths (C12, C16).
  • Analyzed lipid droplet count, area, and subcellular localization.

Main Results:

  • FA uptake was sensitive to acyl chain length and media exposure in trophoblasts.
  • Combined high glucose and high lipid exposure increased mitochondrial protein but impaired respiratory capacity and reduced viability due to apoptosis.
  • Trophoblasts exposed to combined conditions showed reduced uptake of BODIPY C16 into cells and lipid droplets, with altered lipid droplet characteristics, unlike individual exposures.

Conclusions:

  • Combined high glucose and lipid conditions in GDM significantly disrupt placental FA transport and lipid droplet dynamics.
  • These disruptions impair trophoblast function and viability, potentially explaining LCPUFA deficiency in neonates.
  • Findings highlight the complex impact of GDM on placental lipid metabolism, contributing to adverse pregnancy outcomes.

Keywords:
fatty acidsgestational diabetes mellituslipid dropletsmitochondriatrophoblast

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