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Prenatal Exposure to Ethanol and Disturbances in Hepatic One Carbon Metabolism
Author(s) -
Sulistyoningrum Dian C,
Innis Sheila M,
Weinberg Joanne,
Devlin Angela M
Publication year - 2010
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.24.1_supplement.344.1
Subject(s) - offspring , medicine , endocrinology , in utero , liquid diet , fetal alcohol syndrome , ethanol , pregnancy , gestation , methionine , homocysteine , methionine synthase , ethanol metabolism , fetus , metabolism , chemistry , biology , biochemistry , genetics , amino acid
Disturbances in one carbon metabolism contribute to the pathology of adult alcoholic liver disease. We hypothesize that disturbances in one carbon metabolism may contribute to the pathology associated with prenatal ethanol exposure including fetal alcohol spectrum disorder. We studied offspring at gestational age 21 days (GD 21) from female Sprague‐Dawley rats fed a liquid ethanol diet (36% energy from ethanol), a liquid control diet (maltose‐dextrin isocalorically substituted for ethanol, g/kg body wt/day of gestation), or lab chow throughout pregnancy. Liver methionine levels were higher (P< 0.05) and dimethylglycine levels lower (P<0.01) in pups exposed in utero to ethanol than in pups from lab chow‐fed dams. This was accompanied by higher (P<0.05) levels of methionineadenosyltransferase 2a ( Mat2a ), methionine synthase ( Mtr ), methylenetetrahydrofolate reductase ( Mthfr ), and cysthationine‐β‐synthase ( Cbs ) mRNA levels in liver from pups exposed in utero to ethanol than in pups from dams fed lab chow. No effects of prenatal ethanol exposure on betaine‐homocysteine methyltransferase, phosphatidylethanolamine methyltransferase, and Mat1a mRNA levels or Cbs protein levels were observed. These finding suggest that prenatal exposure to ethanol affects liver one carbon metabolism in GD21 offspring.