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Increased placental nutrient transport in a novel mouse model of maternal obesity with fetal overgrowth
Author(s) -
Rosario Fredrick J.,
Kanai Yoshikatsu,
Powell Theresa L.,
Jansson Thomas
Publication year - 2015
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.21165
Subject(s) - endocrinology , medicine , glucose transporter , leptin , fetus , adiponectin , placenta , obesity , pregnancy , amino acid transporter , transporter , insulin , biology , chemistry , insulin resistance , biochemistry , gene , genetics
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.