期刊
OBESITY
卷 23, 期 8, 页码 1663-1670出版社
WILEY
DOI: 10.1002/oby.21165
关键词
-
资金
- NIH [OD016724]
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [R24OD016724] Funding Source: NIH RePORTER
ObjectiveTo 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. MethodsC57BL/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. ResultsHF/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. ConclusionsUp-regulation of specific placental nutrient transporter isoforms may constitute a mechanism underlying fetal overgrowth in maternal obesity.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据