Maternal malnutrition impacts placental morphology and transporter expression: an origin for poor offspring growth

J Nutr Biochem. 2020 Apr:78:108329. doi: 10.1016/j.jnutbio.2019.108329. Epub 2020 Jan 8.

Abstract

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 Fabppm 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.

Keywords: Development; Malnutrition; Morphology; Placenta; Transport.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cadherins / metabolism
  • Connexins / metabolism
  • Cytokines / metabolism
  • Diet, High-Fat / adverse effects
  • Fatty Acid Transport Proteins / metabolism
  • Fatty Acids / metabolism
  • Female
  • Fetal Development
  • Fetal Weight
  • In Situ Hybridization
  • Malnutrition / physiopathology*
  • Maternal Nutritional Physiological Phenomena*
  • Mice
  • Mice, Inbred C57BL
  • Placenta / metabolism
  • Placenta / physiopathology*
  • Pregnancy
  • Pregnancy, Animal
  • Protocadherins
  • RNA, Messenger / metabolism
  • Trophoblasts / metabolism

Substances

  • Cadherins
  • Connexins
  • Cytokines
  • Fatty Acid Transport Proteins
  • Fatty Acids
  • Pcdh12 protein, mouse
  • Protocadherins
  • RNA, Messenger
  • Slc27a4 protein, mouse
  • connexin 31, mouse