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Chronic maternal infusion of full‐length adiponectin in pregnant mice down‐regulates placental amino acid transporter activity and expression and decreases fetal growth
Author(s) -
Rosario Fredrick J,
Schumacher Michael A.,
Jiang Jean,
Kanai Yoshikatsu,
Powell Theresa L.,
Jansson Thomas
Publication year - 2012
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.226399
Subject(s) - medicine , endocrinology , adiponectin , placenta , amino acid transporter , conceptus , fetus , amino acid , transporter , receptor , biology , chemistry , pregnancy , insulin , biochemistry , gene , insulin resistance , genetics
Key points • Fetal growth is positively correlated to maternal adiposity, but the underlying mechanisms remain largely unknown. • Maternal circulating levels of adiponectin, a hormone secreted by adipose tissue, are negatively correlated to maternal adiposity and fetal growth, suggesting that maternal adiponectin may limit fetal growth. • Here we report that chronic administration of adiponectin to pregnant mice inhibits placental insulin and mammalian target of rapamycin (mTOR) signalling, down‐regulates the activity and expression of key placental nutrient transporters, and decreases fetal growth. • We have identified a novel physiological mechanism by which the endocrine functions of maternal adipose tissue influence fetal growth by altering placental function. • These findings may help us better understand the factors determining birth weight in normal pregnancies and in pregnancy complications associated with altered maternal adiponectin levels such as obesity and gestational diabetes.