The effect of pre-existing maternal obesity and diabetes on placental mitochondrial content and electron transport chain activity
Abstract
Introduction Mitochondria dysfunction has been extensively implicated in the progression of these metabolic disorders, their role in placental tissue of diabetic and/or obese pregnant women is yet to be investigated. The aim of this study was to determine the effect of pre-existing type 1 and type 2 diabetes mellitus (DM), and pre-existing maternal obesity on placental mitochondrial function as assessed by mitochondrial content, electron transport chain (ETC) complex activities and oxidative stress.Methods Human placenta was obtained at the time of term Caesarean section from (i) non-obese (n = 19) and obese (n = 23) normal glucose tolerant (NGT) pregnant women; (ii) women with type 1 DM (n = 14) and BMI-matched NGT women (n = 14); and (iii) women with type 2 DM (n = 11) and BMI-matched NGT women (n = 11). The following endpoints were assessed: placental mitochondrial content by citrate synthase activity and mitochondrial DNA (mtDNA content); mitochondrial respiratory chain activity (complexes I, II, II & III, III and IV), and mitochondrial ROS (as assessed by mitochondrial hydrogen peroxide (H2O2) levels).Results When compared to placenta from NGT non-obese women, there was significantly lower mitochondrial DNA (mtDNA) content and electron transport chain complex I activity, and significantly higher mitochondrial H2O2 levels in placenta from NGT obese women (P < 0.05). Placental tissue from type 1 DM women showed significant reductions in ETC complex I, II & III, and III activity and increased H2O2 levels when compared to BMI-matched NGT women (P < 0.05). Type 2 DM women only exhibited significantly reduced ETC complex II & III activity when compared to BMI-matched NGT women (P < 0.05).Discussion and conclusions Women with pre-existing obesity or diabetes have decreased placental mitochondrial respiratory chain enzyme activities which may have detrimental consequences on placental function and therefore fetal growth and development.
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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 [244]
The specific changes in placental ETS function in obese women appear to depend, in part, on the degree of maternal glucose intolerance.
“Certainly, the specific changes in placental ETS function in obese women appear to depend, in part, on the degree of maternal glucose intolerance (244).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [244]
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 [244]
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- Authors
- Hastie, R., & Lappas, M.
- Affiliations
- The University of Melbourne (AU)
- Corresponding author
- Lappas, M.
- ORCID
- Venue
- Placenta
- Publisher
- Elsevier BV
- Published
- 2014-09
- Volume
- 35
- Issue
- 9
- Pages
- 673-683
- ISSN
- 0143-4004 (ISSN-L)
- OpenAlex
- W2046283539
- Cited by
- 107
- References
- 65
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 6 · 2023: 7 · 2022: 11 · 2021: 8 · 2020: 20 · 2019: 6 · 2018: 9 · 2017: 7 · 2016: 7 · 2015: 12 · 2014: 3
- FWCI
- 10.26
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Placenta (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Keywords
- maternal obesity, type 1 diabetes, type 2 diabetes, placental mitochondria, mitochondrial dysfunction, respiratory chain complexes, mitochondrial DNA content, oxidative stress, mitochondrial hydrogen peroxide, citrate synthase, placental function, pregnancy
- MeSH terms
- Adult, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Electron Transport, Female, Humans, Mitochondria, Obesity, Placenta, Pregnancy, Pregnancy in Diabetics, Case-Control Studies, Reactive Oxygen Species, Cell Respiration
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