Diet‐induced obesity in mice reduces placental efficiency and inhibits placental mTOR signaling

Physiological Reports

Susanne Lager¹  Anne-Maj Samulesson²  Paul D. Taylor²  Lucilla Poston²  Theresa L. Powell¹ 

[1]Department of Obstetrics and Gynecology, Center for Pregnancy and Newborn Research, University of Texas Health Science Center, San Antonio, Texas

[2]Division of Women's Health, Women's Health Academic Centre, King's College London and King's Health Partners, London, UK

关键词: Cell signaling;    inflammation;    insulin;    pregnancy;   

DOI  :  10.1002/phy2.242

来源: Wiley

【 摘 要 】

Abstract

As in humans, obesity during pregnancy in mice results in elevated maternal insulin levels and metabolic programming of offspring. mTOR signaling regulates amino acid transport and may function as a placental nutrient sensor. Because obesity is a condition with increased nutrient availability, we hypothesized that diet-induced obesity activates placental mTOR signaling. To test this hypothesis, female C57BL/6J mice were fed an obesogenic diet or standard chow prior to and throughout pregnancy. Fetuses and placentas were collected at gestational day 18. Using Western blot analysis, placental mTOR activity was determined along with energy, inflammatory, and insulin signaling pathways (upstream modulators of mTOR). At gestational day 18, fetal and placental weights did not differ, however, in obese dams, the fetal/placental weight ratio was lower (P < 0.01). In placentas from obese dams, mTOR signaling was inhibited, as determined by decreased Rheb and S6K1 expression, and lower rpS6 phosphorylation (P < 0.05). In contrast, energy, inflammatory, and insulin signaling pathways were unaffected. Contrary to our hypothesis, diet-induced obesity in pregnant mice was associated with inhibition of placental mTOR signaling. However, this finding is consistent with the lower fetal/placental weight ratio, indicating reduced placental efficiency.

【 授权许可】

CC BY   
© 2014 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.