Ethanolamine is a metabolite of the nonessential amino acid serine. In the presence of adequate levels of functional B-6 (P-5-P) serine is enzymatically converted to ethanolamine.
Ethanolamine occurs in every cell in the human body as the head group of Phosphatidylethanolamine (and other lipids), and it is present as free ethanolamine at varying concentrations in bodily fluids. For example, the concentration of ethanolamine in the blood and breast milk is 2 μM (range 0–12 μM) and 46 μM, respectively, whereas the concentration is likely much higher in the gastrointestinal tract due to the breakdown of PE derived from ingested food and the turnover/exfoliation of intestinal epithelial cells.
What is Phosphatidylethanolamine?
Phosphatidylethanolamine (PE) is the second most abundant phospholipid in mammalian cells. PE comprises about 15–25% of the total lipid in mammalian cells; it is enriched in the inner leaflet of membranes, and it is especially abundant in the inner mitochondrial membrane.
References:
Ethanolamine is a metabolite of the nonessential amino acid serine. In the presence of adequate levels of functional B-6 (P-5-P) serine is enzymatically converted to ethanolamine; therefore, ethanolamine could be low as a consequence of P-5-P insufficiency. Alternatively, since serine is derived directly from dietary protein and, endogenously from phosphoserine, glycine and threonine, deficiencies of these precursor metabolites could also result in low levels of ethanolamine. Ethanolamine is important in the body as a precursor of phosphoethanolamine, phosphotidylcholine, choline and the neurotransmitter acetylcholine. Therefore, a deficiency of ethanolamine can be responsible for suppressed activity of the parasympathetic nervous system (eg. GI motility) and poor memory and cognitive function. Symptoms can vary as a function of dietary intake of phosphotidylcholine (lecithin) as a source of choline. Low ethanolamine is usually associated with insufficient protein intake.
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Ethanolamine is a metabolite of serine metabolism. Ethanolamine and phosphoethanolamine are precursors of the neurotransmitter acetycholine. The conversion of ethanolamine to phosphoethanolamine involves a magnesium dependent kinase. When ethanolamine is high or normal and phosphoethanolamine is low, there is a presumptive need for magnesium. Ethanolamine can also be a product of bacterial infection in the urinary tract or the intestine (dysbiosis).
Could be high due to a sluggish conversion of this serine derivative to phosphoethanolamine, possibly reducing acetylcholine synthesis. Supplement magnesium, a main cofactor for this conversion.
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1-Methylhistidine (Plasma), 3-Methylhistidine (Plasma), Alanine (Plasma), Alpha-Amino-n-butyric acid (Plasma), Alpha-Aminoadipic Acid (Plasma), Alpha-ANB/Leucine, Anserine (Plasma), Arginine (Plasma), Asparagine (Plasma), Aspartic Acid (Plasma), Beta-Alanine, Beta-Aminoisobutyric Acid (Plasma), Carnosine (Plasma), Citrulline, Cystathionine (Plasma), Cystine, Ethanolamine (Plasma), g-Aminobutyric Acid (Plasma), Glutamic Acid (Plasma), Glutamic Acid/Glutamine, Glutamine (Plasma), Glycine (Plasma), Histidine (Plasma), Homocysteine (Genova), Homocystine (Genova), Hydroxylysine (Genova), Hydroxyproline (Genova), Hydroxyproline/Proline (Genova), Isoleucine (Plasma), Leucine (Plasma), Lysine (Plasma), Methionine (Plasma), Ornithine (Genova), Phenylalanine (Plasma), Phenylalanine/Tyrosine (Genova), Phosphoethanolamine (Plasma), Phosphoserine (Plasma), Proline (Plasma), Sarcosine (Plasma), Serine (Plasma), Taurine (Plasma), Threonine (Plasma), Tryptophan (Plasma), Tryptophan/LNAA (Genova), Tyrosine (Plasma), Valine (Plasma)
