Metabolic conversion of intra-amniotically-injected deuterium-labeled essential fatty acids by fetal rats following maternal n-3 fatty acid deficiency.
Ephraim Yavin, Yu Hong Lin, Annette Brand, Norman Salem
Index: Biochim. Biophys. Acta 1841(9) , 1336-44, (2014)
Full Text: HTML
Abstract
Accumulation of polyunsaturated fatty acids (PUFA) in the fetal brain is accomplished predominantly via a highly selective flow of docosahexaenoic acid (22:6n-3, DHA) and arachidonic acid (20:4n-6, AA) through the placenta. Little is known regarding the endogenous capability of the fetus to generate its own DHA and AA from lower homologues such as linolenic (18:3n-3, ALA) and linoleic (18:2n-6, LA) acids, respectively. Deuterium-labeled d5-ALA and d5-LA at millimolar concentrations were injected directly into the amniotic fluid in order to investigate maternal-independent metabolic conversion of the stable isotopes in brain and liver of the fetus near delivery. After 48h under adequate maternal diet, the levels of d5-ALA metabolites in the fetal brain and fetal liver were 45±2.2 pmol/mg and 86±4 pmol/mg of which 79% and 63.6% were comprised of d5-DHA. At this time point, incorporation of d5-LA metabolites was 103±5 pmol/mg and 772±46 pmol/mg for brain and liver, of which 50% and 30% were comprised of d5-AA. Following sustained maternal dietary ALA deficiency, the levels of total d5-ALA derived metabolites in the fetal brain and fetal liver were increased to 231 pmol/mg and 696 pmol/mg of which 71% and 26% were comprised of d5-DHA. From the time course and relative rates of d5-ALA precursor displacement by d5-DHA in cellular phosphoglycerides, it is concluded that the fetal rat brain can generate its own DHA from its d5-ALA precursors particularly under dietary stress. Copyright © 2014 Elsevier B.V. All rights reserved.
Related Compounds
Related Articles:
Imaging of a clinically relevant stroke model: glucose hypermetabolism revisited.
2015-03-01
[Stroke 46(3) , 835-42, (2015)]
Suppression of the HSF1-mediated proteotoxic stress response by the metabolic stress sensor AMPK.
2015-02-03
[EMBO J. 34(3) , 275-93, (2015)]
Detailed characterization of a long-term rodent model of critical illness and recovery.
2015-03-01
[Crit. Care Med. 43(3) , e84-96, (2015)]
The chemokine (CCL2-CCR2) signaling axis mediates perineural invasion.
2015-02-01
[Mol. Cancer Res. 13(2) , 380-90, (2015)]
Developmental tightening of cerebellar cortical synaptic influx-release coupling.
2015-02-04
[J. Neurosci. 35(5) , 1858-71, (2015)]