Lysine deprivation during maternal consumption of low-protein diets could adversely affect early embryo development and health in adulthood

Lon J. Van Winkle*, Vasiliy Galat, Philip M. Iannaccone

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

The conversion of lysine to glutamate is needed for signaling in all plants and animals. In mouse embryonic stem (mES) cells, and probably their progenitors, endogenous glutamate production and signaling help maintain cellular pluripotency and proliferation, although the source of glutamate is yet to be determined. If the source of glutamate is lysine, then lysine deprivation caused by maternal low-protein diets could alter early embryo development and, consequently, the health of the offspring in adulthood. For these reasons, we measured three pertinent variables in human embryonic stem (hES) cells as a model for the inner cell masses of human blastocysts. We found that RNA encoding the alpha-aminoadipic semialdehyde synthase enzyme, which regulates glutamate production from lysine, was highly expressed in hES cells. Moreover, the mean amount of lysine consumed by hES cells was 50% greater than the mean amount of glutamate they produced, indicating that lysine is likely converted to glutamate in these cells. Finally, hES cells expressed RNA encoding at least two glutamate receptors. Since this may also be the case for hES progenitor cells in blastocysts, further studies are warranted to verify the presence of this signaling process in hES cells and to determine whether lysine deprivation alters early mammalian embryo development.

Original languageEnglish (US)
Article number5462
Pages (from-to)1-9
Number of pages9
JournalInternational journal of environmental research and public health
Volume17
Issue number15
DOIs
StatePublished - Aug 1 2020

Funding

Funding: Studies in the authors’ laboratories were supported, in part, by a grant from the Illinois Regenerative Medicine Institute. In addition, VG was supported by NHLBI, RC1HL100168, and a Stanley Manne Children’s Research Institute Grant. Studies in the authors? laboratories were supported, in part, by a grant from the Illinois Regenerative Medicine Institute. In addition, VG was supported by NHLBI, RC1HL100168, and a Stanley Manne Children?s Research Institute Grant.

Keywords

  • Barker hypothesis
  • Blastocyst
  • Embryo
  • Embryonic stem cells
  • Glutamate signaling
  • Low-protein diet
  • Lysine
  • Offspring

ASJC Scopus subject areas

  • Pollution
  • Public Health, Environmental and Occupational Health
  • Health, Toxicology and Mutagenesis

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