Increased Placental Nutrient Transport in a Novel Mouse Model of Maternal Obesity with Fetal Overgrowth
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Objective: To identify possible mechanisms linking obesity in pregnancy to increased fetal adiposity and growth, a unique mouse model of maternal obesity associated with fetal overgrowth was developed, and the hypothesis that maternal obesity causes up‐regulation of placental nutrient transporter expression and activity was tested. Methods: C57BL/6J female mice were fed a control (C) or a high‐fat/high‐sugar (HF/HS) pelleted diet supplemented by ad libitum access to sucrose (20%) solution, mated, and studied at embryonic day 18.5. Results: HF/HS diet increased maternal fat mass by 2.2‐fold (P < 0.01) and resulted in glucose intolerance with normal fasting glucose. Maternal circulating insulin, leptin, and cholesterol were increased (P < 0.05) whereas total and high‐molecular‐weight adiponectin was decreased (P < 0.05). HF/HS diet increased fetal weight (+18%, P = 0.0005). In trophoblast plasma membranes (TPM) isolated from placentas of HF/HS‐fed animals, protein expression of glucose transporter (GLUT) 1 and 3, sodium‐coupled neutral amino acid transporter (SNAT) 2, and large neutral amino acid transporter 1 (LAT1) was increased. TPM System A and L amino acid transporter activity was increased in the HF/HS group. Conclusions: Up‐regulation of specific placental nutrient transporter isoforms may constitute a mechanism underlying fetal overgrowth in maternal obesity.
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Maternal obesity is associated with increased placental nutrient transport capacity.
“Maternal obesity has been associated with increased placental nutrient transport capacity, although the underlying biochemical mechanisms remain unclear.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [52]
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- Authors
- Rosario, F. J., Kanai, Y., Powell, T. L., & Jansson, T.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- The University of Osaka (JP)
- University of Colorado Anschutz (US)
- Corresponding author
- Rosario, Fredrick J.
- Venue
- Obesity
- Publisher
- Wiley
- Published
- 2015-07-20
- Volume
- 23
- Issue
- 8
- Pages
- 1663-1670
- ISSN
- 1930-7381 (ISSN-L)
- 1930-739X
- PMC
- PMC4509489
- OpenAlex
- W1529979603
- Cited by
- 128
- References
- 38
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 14 · 2023: 10 · 2022: 16 · 2021: 12 · 2020: 18 · 2019: 15 · 2018: 9 · 2017: 10 · 2016: 3 · 2015: 6
- FWCI
- 10.62
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Obesity (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (OD016724)
- Topics
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Keywords
- maternal obesity, fetal overgrowth, placental nutrient transport, nutrient transporters, high-fat high-sugar diet, sucrose, glucose transporter 1, GLUT3, SNAT2, LAT1, amino acid transporters, adiponectin, leptin, insulin, impaired glucose tolerance, fetal adiposity, mouse model
- MeSH terms
- Animals, Disease Models, Animal, Female, Insulin, Mice, Inbred C57BL, Mothers, Obesity, Pregnancy, Weight Gain, Up-Regulation, Fetal Weight, Leptin, Mice
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