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

2 Citations (Scopus)

Abstract

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
JournalPlacenta
Volume69
DOIs
StatePublished - Sep 1 2018

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Carnitine
Fatty Acids
Trophoblasts
Transforming Growth Factors
Placenta
Intercellular Signaling Peptides and Proteins
Mitochondria
Genes

ASJC Scopus subject areas

  • Reproductive Medicine
  • Obstetrics and Gynecology
  • Developmental Biology

Cite this

Embryonic lethality in mice due to carnitine transporter OCTN2 defect and placental carnitine deficiency. / Shekhawat, Prem S.; Sonne, Srinivas; Matern, Dietrich; Ganapathy, Vadivel.

In: Placenta, Vol. 69, 01.09.2018, p. 71-73.

Research output: Contribution to journalArticle

Shekhawat, Prem S. ; Sonne, Srinivas ; Matern, Dietrich ; Ganapathy, Vadivel. / Embryonic lethality in mice due to carnitine transporter OCTN2 defect and placental carnitine deficiency. In: Placenta. 2018 ; Vol. 69. pp. 71-73.
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