Cited by 129Gestational Diabetes Research and ManagementBirth, Development, and HealthPregnancy and preeclampsia studies

Increased Placental Nutrient Transport in a Novel Mouse Model of Maternal Obesity with Fetal Overgrowth

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Rosario, Fredrick J., Kanai, Yoshikatsu, Powell, Theresa L., Jansson, Thomas·2015·Obesity

Abstract

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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  1. [35]Pedersen J Weight and length at birth of infants of diabetic mothers Acta Endocrinol 1954 3303 42 13206643

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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
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
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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