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Phosphatidylethanolamine N‐methyltransferase (PEMT) activity in pregnant and postpartum mice fed a control or choline‐deficient diet
Author(s) -
Knight Elizabeth R,
Mehedint Mihai G.,
Craciunescu Corneliu N.,
Costa KerryAnn da,
Zeisel Steven H.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a572-c
Subject(s) - choline , endocrinology , medicine , lactation , estrogen , fetus , pregnancy , biology , offspring , methionine , biochemistry , amino acid , genetics
Choline is an important nutrient during pregnancy and lactation when choline transport from mother to fetus supports fetal brain development. Choline is derived from the diet and from an endogenous pathway where phosphatidylethanolamine N ‐methyltransferase (PEMT) methylates phosphatidylethanolamine using S‐adenosyl‐L‐methionine (SAM) as the methyl donor. Previous research shows that PEMT activity is increased by estrogen and by a choline‐deficient diet. Pregnancy increases maternal serum estrogen levels and depletes maternal liver of choline. We investigated PEMT activity in pregnant or postpartum C57BL/6J mice fed either a control or choline‐deficient diet. Hepatic PEMT activity was measured at embryonic days 15 and 18 (E15, E18) and 1, 15, and 30 days postpartum (P1, P15, P30) using a radioenzymatic assay. PEMT activity across these time points did not statistically change in dam liver from either the control or choline‐deficient group. Also, changes in Pemt gene expression were measured with real‐time PCR, using β‐actin as an endogenous control gene. In the control diet group, Pemt gene expression at both E18 and P1 was significantly higher than at P15 and P30 (P< 0.05). In the choline‐deficient group, Pemt expression at both E18 and P1 was significantly higher than expression at P15 (P<0.05). These results demonstrate that pregnancy has differential effects on Pemt gene expression in dam liver. This research was supported by grants from Mead Johnson Nutritionals and NIH (DK55865 and AG09525).