Placental Amino Acid Transport and Placental Leptin Resistance in Pregnancies Complicated by Maternal Obesity
Abstract
Unlabelled HYPOTHESIS AND STUDY OBJECTIVES: We hypothesized that maternal obesity is associated with increased placental amino acid transport and hyperleptinemia. Our objectives were to study placental amino acid transport and the effect of leptin on placental amino acid transport in vitro in the setting of maternal obesity.Materials and methods Seven lean, BMI at entry 22.4, and seven obese, BMI at entry 31.5 (p < 0.001), pregnant women were studied at 39 weeks. We measured baseline and leptin-stimulated placental system A sodium-dependent neutral amino acid transporter (SNAT) activity, placental immunoreactive protein expression of SNAT, leptin and leptin receptor, and maternal and fetal plasma leptin concentrations, with significance set at p <or= 0.05. The primary outcome measure was placental SNAT activity.Results The obese group had decreased placental SNAT activity (p = 0.005), maternal hyperleptinemia (p = 0.01) and decreased syncytiotrophoblast expression of leptin receptor (p = 0.01) and SNAT-4 (p < 0.001). Placental amino acid uptake was significantly stimulated by leptin in the lean group as compared to the obese group. Maternal weight gain and offspring birth weights were not different between groups.Conclusion Maternal obesity was accompanied by decreased placental SNAT activity associated with maternal hyperleptinemia and placental leptin resistance in spite of appropriate maternal weight gain and normally grown neonates. These findings suggest altered placental function that may have clinical implications in obese pregnant women.
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Reduced taurine and System A transport activity, and lower SNAT4 expression, are seen in placental villous fragments from obese women delivering infants of normal birth weight.
“Reduced taurine and System A transport activity, and lower SNAT4 expression, are also seen in placental villous fragments from obese women delivering infants of normal birth weight (151, 184).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [184]
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- Authors
- Farley, D. M., Choi, J., Dudley, D. J., Li, C., Jenkins, S. L., Myatt, L., & Nathanielsz, P. W.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Corresponding author
- Farley, D.M.
- Venue
- Placenta
- Publisher
- Elsevier BV
- Published
- 2010-08
- Volume
- 31
- Issue
- 8
- Pages
- 718-724
- ISSN
- 0143-4004 (ISSN-L)
- OpenAlex
- W2051733253
- Cited by
- 150
- References
- 42
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 5 · 2023: 6 · 2022: 11 · 2021: 9 · 2020: 6 · 2019: 12 · 2018: 7 · 2017: 12 · 2016: 11 · 2015: 17 · 2014: 17 · 2013: 13 · 2012: 11
- FWCI
- 12.92
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Placenta (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Texas at San Antonio
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD 21350-17, P01HD021350)
- Topics
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Keywords
- maternal obesity, placental amino acid transport, leptin resistance, hyperleptinemia, leptin receptor, syncytiotrophoblast, placental function, pregnancy, fetal growth
- MeSH terms
- Female, Humans, Immunohistochemistry, Infant, Newborn, Insulin, Obesity, Placenta, Pregnancy, Pregnancy Complications, Body Mass Index, Leptin, Amino Acid Transport System A
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