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Physiological changes in maternal glucose levels in pregnancies complicated by diabetes impact the human placental transcriptome

ABSTRACT: Recent continuous glucose monitoring (CGM) studies have revealed that in pregnancies complicated by maternal diabetes, fluctuations in maternal glucose are linked to complications of fetal growth. The underlying mechanisms are unclear but likely involve the placenta. We cultured ex vivo human placental explants from term uncomplicated pregnancies with medium changes every 6-18 hours in variable (5/5.5 mM; normoglycaemia), or constant 5 mM (mild hypoglycaemia) or 7 mM glucose (mild hyperglycaemia) for 48 hours to recapitulate in vivo maternal glucose profiles and performed RNA sequencing. Additional placental explants were also exposed to 5.5 mM glucose.

ORGANISM(S): Homo sapiens

PROVIDER: GSE288239 | GEO | 2025/06/18

REPOSITORIES: GEO

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Project description:Pre-existing and gestationally-developed diabetes mellitus during pregnancy have been linked to impaired metabolic function in the villous trophoblast layer of the placenta. These metabolic impairments have been thought to mediate an increased risk of early life metabolic disease development in the exposed offspring. Previous research using the BeWo trophoblast cell line has suggested that independently, hyperglycemia is an important modulator of placental metabolic function in diabetic pregnancies. However, the direct impacts of hyperglycemia on specific aspects of placental metabolic function known to be impaired in diabetic pregnancies including nutrient storage and mitochondrial respiration, are largely unknown. The current study, therefore, utilized functional readouts of metabolic enzyme activity and endpoint readouts of nutrient storage in conjunction with multi-omics analysis (transcriptomics and metabolomics) in BeWo trophoblasts cultured under hyperglycemia conditions (25 mM glucose) for 72 hours to further characterize the impacts of elevated glucose levels on placental metabolic function. While metabolic enzyme activities and mitochondrial oxidative respiratory function were not altered following 72 hours of hyperglycemia, increased triglyceride and glycogen nutrient stores were observed in the high-glucose exposed BeWo trophoblasts. We speculated that the increased nutrient stores serve to modulate intracellular glucose levels and may reduce the amount of glucose available for oxidation and subsequently protect trophoblast cells from mitochondrial damage during acute high glucose exposures. Additionally, hyperglycemic-culture conditions in BeWo trophoblasts were associated with an altered transcriptomic profile highlighted by altered mRNA expression of metabolic enzymes as well as with an altered metabolome profile highlighted by an intracellular accumulation of lactate, malonate, and riboflavin. Overall, the results demonstrate that exposure to excess glucose modulates placental metabolism and nutrient storage and highlights that increased glucose abundance is an important independent regulator of placental function in diabetic pregnancies.

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Physiological changes in maternal glucose levels in pregnancies complicated by diabetes impact the human placental transcriptome

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