Biosynthesis Biosynthesis of<unk>  in plants In plants, the first step in de novo biosynthesis of<unk>  is the decarboxylation of serine into ethanolamine, which is catalyzed by a serine decarboxylase. The synthesis of<unk>  from ethanolamine may take place in three parallel pathways, where three consecutive N-methylation steps catalyzed by a methyl transferase are carried out on either the free-base, phospho-bases, or phosphatidyl-bases. The source of the methyl group is S-adenosyl--methionine and S-adenosyl--homocysteine is generated as a side product. Main pathways of<unk>  <unk> ol) metabolism, synthesis and excretion. Click for details. Some of the abbreviations are used in this section. In humans and most other animals, de novo synthesis of<unk>  is via the phosphatidylethanolamine N-methyltransferase (PEMT) pathway, but biosynthesis is not enough to meet human requirements. In the hepatic PEMT route, 3-phosphoglycerate (3PG) receives 2 acyl groups from acyl-CoA forming a phosphatidic acid. It reacts with cytidine triphosphate to form cytidine diphosphate-diacylglycerol. Its hydroxyl group reacts with serine to form phosphatidylserine which decarboxylates to ethanolamine and phosphatidylethanolamine (PE) forms. A PEMT enzyme moves three methyl groups from three S-adenosyl methionines (SAM) donors to the ethanolamine group of the phosphatidylethanolamine to form<unk>  in the form of a phosphatidylcholine. Three S-adenosylhomocysteines (SAHs) are formed as a byproduct.<unk>  can also be released from more complex<unk>  containing molecules. For example, phosphatidylcholines (PC) can be hydrolyzed to<unk>  <unk> ol) in most cell types.<unk>  can also be produced by the CDP-choline route, cytosolic<unk>  kinases (CK) phosphorylate<unk>  with ATP to phosphocholine (PChol). This happens in some cell types like liver and kidney.<unk> -phosphate cytidylyltransferases (CPCT) transform PChol to CDP-choline (CDP-Chol) with cytidine triphosphate (CTP). CDP-choline and diglyceride are transformed to PC by diacylglycerol<unk> phosphotransferase (CPT). In humans, certain PEMT-enzyme mutations and estrogen deficiency (often due to menopause) increase the dietary need for<unk> . In rodents, 70% of phosphatidylcholines are formed via the PEMT route and only 30% via the CDP-choline route. In knockout mice, PEMT inactivation makes them completely dependent on dietary<unk> . Absorption In humans,<unk>  is absorbed from the intestines via the SLC44A1 (CTL1) membrane protein via facilitated diffusion governed by the<unk>  concentration gradient and the electrical potential across the enterocyte membranes. SLC44A1 has limited ability to transport<unk> : at high concentrations part of it is left unabsorbed. Absorbed<unk>  leaves the enterocytes via the portal vein, passes the liver and enters systemic circulation. Gut microbes degrade the unabsorbed<unk>  to trimethylamine, which is oxidized in the liver to trimethylamine N-oxide. Phosphocholine and glycerophosphocholines are hydrolyzed via phospholipases to<unk> , which enters the portal vein. Due to their water solubility, some of them escape unchanged to the portal vein. Fat-soluble<unk> -containing compounds (phosphatidylcholines and sphingomyelins) are either hydrolyzed by phospholipases or enter the lymph incorporated into<unk> ylomicrons. Transport In humans,<unk>  is transported as a free molecule in blood.<unk> –containing phospholipids and other substances, like glycerophosphocholines, are transported in blood lipoproteins. Blood plasma<unk>  levels in healthy fasting adults is 7–20 micromoles per liter (μmol/l) and 10 μmol/l on average. Levels are regulated, but<unk>  intake and deficiency alters these levels. Levels are elevated for about 3 hours after<unk>  consumption. Phosphatidylcholine levels in the plasma of fasting adults is 1.5–2.5 mmol/l. Its consumption elevates the free<unk>  levels for about 8–12 hours, but does not affect phosphatidylcholine levels significantly.<unk>  is a water-soluble ion and thus requires transporters to pass through fat-soluble cell membranes. Three types of<unk>  transporters are known: *SLC5A7 *CTLs: CTL1 (SLC44A1), CTL2 (SLC44A2) and CTL4 (SLC44A4) *OCTs: OCT1 (SLC22A1) and OCT2 (SLC22A2) SLC5A7s are sodium- (Na+) and ATP-dependent transporters. They have high binding affinity for<unk> , transport it primarily to neurons and are indirectly associated with the acetylcholine production. Their deficient function causes hereditary weakness in the pulmonary and other muscles in humans via acetylcholine deficiency. In knockout mice, their dysfunction results easily in death with cyanosis and paralysis. CTL1s have moderate affinity for<unk>  and transport it in almost all tissues, including the intestines, liver, kidneys, placenta and mitochondria. CTL1s supply<unk>  for phosphatidylcholine and trimethylglycine production. CTL2s occur especially in the mitochondria in the tongue, kidneys, muscles and heart. They are associated with the mitochondrial oxidation of<unk>  to trimethylglycine. CTL1s and CTL2s are not associated with the acetylcholine production, but transport<unk>  together via the blood–brain barrier. Only CTL2s occur on the brain side of the barrier. They also remove excess<unk>  from the neurons back to blood. CTL1s occur only on the blood side of the barrier, but also on the membranes of astrocytes and neurons. OCT1s and OCT2s are not associated with the acetylcholine production. They transport<unk>  with low affinity. OCT1s transport<unk>  primarily in the liver and kidneys; OCT2s in kidneys and the brain. Storage<unk>  is stored in the cell membranes and organelles as phospholipids, and inside cells as phosphatidylcholines and glycerophosphocholines. Excretion Even at<unk>  doses of 2–8 g, little<unk>  is excreted into urine in humans. Excretion happens via transporters that occur within kidneys (see transport). Trimethylglycine is demethylated in the liver and kidneys to dimethylglycine (tetrahydrofolate receives one of the methyl groups). Methylglycine forms, is excreted into urine, or is demethylated to glycine.
Choline
Phenylacetic acid
Arachidonic acid
Keto acid
Gluten
Butyric acid
Palate
Inositol