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

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

doi:10.1016/j.placenta.2018.06.312

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

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

Laboratory Medicine and Pathology

Research output: Contribution to journal › Article › peer-review

4 Scopus citations

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 language	English (US)
Pages (from-to)	71-73
Number of pages	3
Journal	Placenta
Volume	69
DOIs	https://doi.org/10.1016/j.placenta.2018.06.312
State	Published - Sep 2018

ASJC Scopus subject areas

Reproductive Medicine
Obstetrics and Gynecology
Developmental Biology

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title = "Embryonic lethality in mice due to carnitine transporter OCTN2 defect and placental carnitine deficiency",

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.",

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AU - Shekhawat, Prem S.

AU - Sonne, Srinivas

AU - Matern, Dietrich

AU - Ganapathy, Vadivel

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AB - 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.

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

Abstract

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