Impaired mitochondrial function in human placenta with increased maternal adiposity
Open accessAbstract
The placenta plays a key role in regulation of fetal growth and development and in mediating in utero developmental programming. Obesity, which is associated with chronic inflammation and mitochondrial dysfunction in many tissues, exerts a programming effect in pregnancy. We determined the effect of increasing maternal adiposity and of fetal sex on placental ATP generation, mitochondrial biogenesis, expression of electron transport chain subunits, and mitochondrial function in isolated trophoblasts. Placental tissue was collected from women with prepregnancy BMI ranging from 18.5 to 45 following C-section at term with no labor. Increasing maternal adiposity was associated with excessive production of reactive oxygen species and a significant reduction in placental ATP levels in placentae with male and female fetuses. To explore the potential mechanism of placental mitochondrial dysfunction, levels of transcription factors regulating the expression of genes involved in electron transport and mitochondrial biogenesis were measured. Our in vitro studies showed significant reduction in mitochondrial respiration in cultured primary trophoblasts with increasing maternal obesity along with an abnormal metabolic flexibility of these cells. This reduction in placental mitochondrial respiration in pregnancies complicated by maternal obesity could compromise placental function and potentially underlie the increased susceptibility of these pregnancies to fetal demise in late gestation and to developmental programming.
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Mitochondrial density and expression of the electron transport chain ETS complexes decrease in the human placenta as maternal BMI increases.
“Furthermore, mitochondrial density and expression of the electron transport chain ETS complexes decrease in the human placenta as maternal BMI increases, with the result that placental respiration is lower in obese than lean women (244, 376).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [376]
Placental respiration is lower in obese than lean women.
“Furthermore, mitochondrial density and expression of the electron transport chain ETS complexes decrease in the human placenta as maternal BMI increases, with the result that placental respiration is lower in obese than lean women (244, 376).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [376]
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- Authors
- Mele, J., Muralimanoharan, S., Maloyan, A., & Myatt, L.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Corresponding author
- Myatt, Leslie
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2014-09-01
- Volume
- 307
- Issue
- 5
- Pages
- E419-E425
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- PMC
- PMC4154072
- OpenAlex
- W2060301363
- Semantic Scholar
- fed5ec549bf327c45f840b6f1ffe832e4f50b1d0
- Cited by
- 163
- References
- 65
- Citations by year
- 2026: 9 · 2025: 14 · 2024: 10 · 2023: 13 · 2022: 15 · 2021: 18 · 2020: 18 · 2019: 17 · 2018: 12 · 2017: 11 · 2016: 13 · 2015: 11 · 2014: 1
- FWCI
- 12.74
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (UL1TR001120, KL2TR001118)
- National Heart, Lung, and Blood Institute (HL075297, R01HL075297)
- National Center for Research Resources (UL1RR025767)
- National Center for Advancing Translational Sciences
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD076259)
- Topics
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Keywords
- maternal obesity, placenta, mitochondrial dysfunction, mitochondrial biogenesis, electron transport chain, trophoblast, ATP production, reactive oxygen species, fetal sex, developmental programming, prepregnancy BMI, mitochondrial respiration, metabolic flexibility, placental function
- MeSH terms
- Adenosine Triphosphate, Adult, Cells, Cultured, Chorionic Villi, Energy Metabolism, Female, Humans, Male, Mitochondria, Obesity, Placenta, Pregnancy, Pregnancy Complications, Body Mass Index, Reactive Oxygen Species, Adiposity
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