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Cited by 227Birth, Development, and HealthPregnancy and preeclampsia studiesGestational Diabetes Research and Management

Placental Function in Maternal Obesity

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Kelly, Amy C., Powell, Theresa L., Jansson, Thomas·2020·Clinical Science
DOI 10.1042/cs20190266PMC PMC8820171
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Abstract

Maternal obesity is associated with pregnancy complications and increases the risk for the infant to develop obesity, diabetes and cardiovascular disease later in life. However, the mechanisms linking the maternal obesogenic environment to adverse short- and long-term outcomes remain poorly understood. As compared with pregnant women with normal BMI, women entering pregnancy obese have more pronounced insulin resistance, higher circulating plasma insulin, leptin, IGF-1, lipids and possibly proinflammatory cytokines and lower plasma adiponectin. Importantly, the changes in maternal levels of nutrients, growth factors and hormones in maternal obesity modulate placental function. For example, high insulin, leptin, IGF-1 and low adiponectin in obese pregnant women activate mTOR signaling in the placenta, promoting protein synthesis, mitochondrial function and nutrient transport. These changes are believed to increase fetal nutrient supply and contribute to fetal overgrowth and/or adiposity in offspring, which increases the risk to develop disease later in life. However, the majority of obese women give birth to normal weight infants and these pregnancies are also associated with activation of inflammatory signaling pathways, oxidative stress, decreased oxidative phosphorylation and lipid accumulation in the placenta. Recent bioinformatics approaches have expanded our understanding of how maternal obesity affects the placenta; however, the link between changes in placental function and adverse outcomes in obese women giving birth to normal sized infants is unclear. Interventions that specifically target placental function, such as activation of placental adiponectin receptors, may prevent the transmission of metabolic disease from obese women to the next generation.

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Authors
Kelly, A. C., Powell, T. L., & Jansson, T.
Affiliations
University of Colorado Anschutz (US)
ORCID
Kelly, Amy C.
Venue
Clinical Science
Publisher
Portland Press Ltd.
Published
2020-04
Volume
134
Issue
8
Pages
961-984
ISSN
  • 0143-5221 (ISSN-L)
  • 1470-8736
DOI
10.1042/cs20190266
PMC
PMC8820171
OpenAlex
W3017172592
Cited by
227
References
22
Citations by year
2026: 33 · 2025: 44 · 2024: 43 · 2023: 50 · 2022: 31 · 2021: 20 · 2020: 6
FWCI
5.88
Type
journal article
Language
en
Open access
Locations
  • Clinical Science (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (5r01hd068370-11)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD078376, R01-HD068370, R03HD093950, R01HD065007, R01HD089980, T32HD007186)
Topics
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
  • Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
Keywords
maternal obesity, placental function, insulin resistance, leptin, insulin-like growth factor I, adiponectin, mTOR signaling, fetal overgrowth, fetal programming, placental inflammation, oxidative stress
MeSH terms
Pregnancy in Obesity, Obesity, Maternal, Animals, Female, Humans, Insulin-Like Growth Factor I, Placenta, Pregnancy, Pregnancy Complications, Adiposity, Adiponectin

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