PMID- 32004932
OWN - NLM
STAT- MEDLINE
DCOM- 20210223
LR  - 20211204
IS  - 1873-4847 (Electronic)
IS  - 0955-2863 (Linking)
VI  - 78
DP  - 2020 Apr
TI  - Maternal malnutrition impacts placental morphology and transporter expression: an 
      origin for poor offspring growth.
PG  - 108329
LID - S0955-2863(19)30740-5 [pii]
LID - 10.1016/j.jnutbio.2019.108329 [doi]
AB  - The placenta promotes fetal growth through nutrient transfer and selective 
      barrier systems. An optimally developed placenta can adapt to changes in the 
      pregnancy environment, buffering the fetus from adverse exposures. We 
      hypothesized that the placenta adapts differently to suboptimal maternal diets, 
      evidenced by changes in placental morphology, developmental markers and key 
      transport systems. Mice were fed a control diet (CON) during pregnancy, 
      undernourished (UN) by 30% of control intake from gestational day (GD) 5.5-18.5 
      or fed 60% high-fat diet (HF) 8 weeks before and during pregnancy. At GD18.5, 
      placental morphometry, development and transport were assessed. Junctional and 
      labyrinthine areas of UN and HF placentae were smaller than CON by >10%. Fetal 
      blood space area and fetal blood space:fetal weight ratios were reduced in HF vs. 
      CON and UN. Trophoblast giant cell marker Ctsq mRNA expression was lower in UN 
      vs. HF, and expression of glycogen cell markers Cx31.1 and Pcdh12 was lower in HF 
      vs. UN. Efflux transporter Abcb1a mRNA expression was lower in HF vs. UN, and 
      Abcg2 expression was lower in UN vs. HF. mRNA expression of fatty acid binding 
      protein Fabp(pm) was higher in UN vs. CON and HF. mRNA and protein levels of the 
      lipid transporter FAT/CD36 were lower in UN, and FATP4 protein levels were lower 
      in HF vs. UN. UN placentae appear less mature with aberrant transport, whereas HF 
      placentae adapt to excessive nutrient supply. Understanding placental adaptations 
      to common nutritional adversities may reveal mechanisms underlying the 
      developmental origins of later disease.
CI  - Copyright (c) 2020 Elsevier Inc. All rights reserved.
FAU - Connor, Kristin L
AU  - Connor KL
AD  - Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, 
      Canada; Health Sciences, Carleton University, Ottawa, Ontario, Canada. Electronic 
      address: kristin.connor@carleton.ca.
FAU - Kibschull, Mark
AU  - Kibschull M
AD  - Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, 
      Canada.
FAU - Matysiak-Zablocki, Elzbieta
AU  - Matysiak-Zablocki E
AD  - Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, 
      Canada.
FAU - Nguyen, Tina Tu-Thu Ngoc
AU  - Nguyen TTN
AD  - Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, 
      Canada.
FAU - Matthews, Stephen G
AU  - Matthews SG
AD  - Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, 
      Canada; Department of Physiology, University of Toronto, Toronto, Ontario, 
      Canada; Department of Obstetrics and Gynaecology, University of Toronto, Toronto, 
      Ontario, Canada.
FAU - Lye, Stephen J
AU  - Lye SJ
AD  - Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, 
      Canada; Department of Physiology, University of Toronto, Toronto, Ontario, 
      Canada; Department of Obstetrics and Gynaecology, University of Toronto, Toronto, 
      Ontario, Canada.
FAU - Bloise, Enrrico
AU  - Bloise E
AD  - Department of Physiology, University of Toronto, Toronto, Ontario, Canada; 
      Department of Morphology, Federal University of Minas Gerais, Belo Horizonte, 
      Brazil.
LA  - eng
GR  - MOP-81238/CIHR/Canada
GR  - FDN-143262/CIHR/Canada
GR  - MFE-246638/CIHR/Canada
GR  - 452740/CIHR/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200108
PL  - United States
TA  - J Nutr Biochem
JT  - The Journal of nutritional biochemistry
JID - 9010081
RN  - 0 (Cadherins)
RN  - 0 (Connexins)
RN  - 0 (Cytokines)
RN  - 0 (Fatty Acid Transport Proteins)
RN  - 0 (Fatty Acids)
RN  - 0 (Pcdh12 protein, mouse)
RN  - 0 (Protocadherins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Slc27a4 protein, mouse)
RN  - 0 (connexin 31, mouse)
SB  - IM
MH  - Animals
MH  - Cadherins/metabolism
MH  - Connexins/metabolism
MH  - Cytokines/metabolism
MH  - Diet, High-Fat/adverse effects
MH  - Fatty Acid Transport Proteins/metabolism
MH  - Fatty Acids/metabolism
MH  - Female
MH  - Fetal Development
MH  - Fetal Weight
MH  - In Situ Hybridization
MH  - Malnutrition/*physiopathology
MH  - *Maternal Nutritional Physiological Phenomena
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Placenta/metabolism/*physiopathology
MH  - Pregnancy
MH  - Pregnancy, Animal
MH  - Protocadherins
MH  - RNA, Messenger/metabolism
MH  - Trophoblasts/metabolism
OTO - NOTNLM
OT  - Development
OT  - Malnutrition
OT  - Morphology
OT  - Placenta
OT  - Transport
COIS- Competing interests The authors have no competing interests and nothing to 
      disclose.
EDAT- 2020/02/01 06:00
MHDA- 2021/02/24 06:00
CRDT- 2020/02/01 06:00
PHST- 2019/08/07 00:00 [received]
PHST- 2019/12/17 00:00 [revised]
PHST- 2019/12/18 00:00 [accepted]
PHST- 2020/02/01 06:00 [pubmed]
PHST- 2021/02/24 06:00 [medline]
PHST- 2020/02/01 06:00 [entrez]
AID - S0955-2863(19)30740-5 [pii]
AID - 10.1016/j.jnutbio.2019.108329 [doi]
PST - ppublish
SO  - J Nutr Biochem. 2020 Apr;78:108329. doi: 10.1016/j.jnutbio.2019.108329. Epub 2020 
      Jan 8.