Embryonic lethality in mice due to carnitine transporter OCTN2 defect and placental carnitine deficiency

Prem S. Shekhawat, Srinivas Sonne, Dietrich Matern, Vadivel Ganapathy

Research output: Contribution to journalArticle

3 Scopus citations


L-Carnitine plays a crucial role in uptake and subsequent β-oxidation of long-chain fatty acids in the mitochondria. Placental trophoblast cells oxidize long-chain fatty acids for energy production. Here we present data showing that L-carnitine deficiency due to a defect in the carnitine transporter OCTN2 (SLC22A5) in a mouse model leads to embryonic lethality. Placental levels of L-carnitine are reduced to <10% of normal and deficiency of L-carnitine is associated with markedly reduced expression of several growth factors and transforming growth factor β (TGF-β) genes. This report links for the first time reduced L-carnitine levels in the placenta to embryonic lethality.

Original languageEnglish (US)
Pages (from-to)71-73
Number of pages3
StatePublished - Sep 1 2018


ASJC Scopus subject areas

  • Reproductive Medicine
  • Obstetrics and Gynecology
  • Developmental Biology

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