Effects of ethanolamine (ETN) Administration on etn and choline (CH) levels in plasma, brain extracellular fluid (ECF) and brain tissue, and on brain phospholipid levels in rats: An in vivo study

Marshall, David L.; Micheli, Enrico De; Богданов, М. Б.; Wurtman, Richard J.

doi:10.1002/(sici)1520-6769(199603)18:2<87::aid-nrc144>3.0.co;2-c

Cited by 12 publications

(5 citation statements)

References 38 publications

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“…One biopsy had choline concentrations approximately five times those of the other two, possibly indicating the occurrence of ischemia in the brain tissue from which the biopsy was taken, since ischemia leads to a rapid rise in tissue free choline concentration (42). However, in two biopsies, tissue choline concentration was approximately 40 µM, a value comparable to that found in rodent brain (30-60 µM (23,24). Thus, under normal conditions, human brain choline kinase may be viewed as a single enzyme half maximally active at choline concentrations of approximately 20 µM (see Fig.…”

Section: Discussionmentioning

confidence: 99%

Phospholipid biosynthetic enzymes in human brain

Ross

Moszczynska²,

Blusztajn

et al. 1997

Lipids

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Growing evidence suggests an involvement of brain membrane phospholipid metabolism in a variety of neurodegenerative and psychiatric conditions. This has prompted the use of drugs (e.g., CDPcholine) aimed at elevating the rate of neural membrane synthesis. However, no information is available regarding the human brain enzymes of phospholipid synthesis which these drugs affect. Thus, the objective of our study was to characterize the enzymes involved, in particular, whether differences existed in the relative affinity of substrates for the enzymes of phosphatidylethanolamine (PE) compared to those of phosphatidylcholine (PC) synthesis. The concentration of choline in rapidly frozen human brain biopsies ranged from 32-186 nmol/g tissue, a concentration similar to that determined previously for ethanolamine. Since human brain ethanolamine kinase possessed a much lower affinity for ethanolamine (Km = 460 microM) than choline kinase did for choline (Km = 17 microM), the activity of ethanolamine kinase in vivo may be more dependent on substrate availability than that of choline kinase. In addition, whereas ethanolamine kinase was inhibited by choline, and to a lesser extent by phosphocholine, choline kinase activity was unaffected by the presence of ethanolamine, or phosphoethanolamine, and only weakly inhibited by phosphocholine. Phosphoethanolamine cytidylyltransferase (PECT) and phosphocholine cytidylyltransferase (PCCT) also displayed dissimilar characteristics, with PECT and PCCT being located predominantly in the cytosolic and particulate fractions, respectively. Both PECT and PCCT exhibited a low affinity for CTP (Km approximately 1.2 mM), suggesting that the activities of these enzymes, and by implication, the rate of phospholipid synthesis, are highly dependent upon the cellular concentration of CTP. In conclusion our data indicate different regulatory properties of PE and PC synthesis in human brain, and suggest that the rate of PE synthesis may be more dependent upon substrate (ethanolamine) availability than that of PC synthesis.

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Section: Discussionmentioning

confidence: 99%

Phospholipid biosynthetic enzymes in human brain

Ross

Moszczynska²,

Blusztajn

et al. 1997

Lipids

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“…Alternatively, Etn may affect brain myoIns levels through indirect mechanisms. Specifically, we know that Etn administration can cause alterations in phospholipid concentrations (12) and choline concentrations (22) in rat brain. How myo-Ins and Etn interact within the brain is unknown; however, there seems to be a relationship between the two substances when in combination.…”

Section: Effects On Myo-ins Concentrationsmentioning

confidence: 98%

Administration of Myo-inositol Plus Ethanolamine Elevates Phosphatidylethanolamine Plasmalogen in the Rat Cerebellum

Hoffman-Kuczynski

Reo

2005

Neurochem Res

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Plasmalogens are ether-linked phospholipids highly abundant in nervous tissue. Previously we demonstrated that acute administration of myo-inositol (myo-Ins) + [2-(13)C] ethanolamine ([2-(13)C]Etn) significantly elevated phosphatidylethanolamine plasmalogen (PlsEtn) in rat whole brain. Current experiments investigated the effects of acute myo-Ins+[2-(13)C]Etn administration on [PlsEtn] and the biosynthesis of new Etn lipids using NMR spectroscopy in rat cerebral cortex, hippocampus, brainstem, midbrain and cerebellum. Treated rats received a single dose of myo-Ins + [2-(13)C]Etn and controls received saline rather than myoIns. Data reveal that the cerebellum is the brain region most affected by treatment, which resulted in a 22% increase in [PlsEtn] and 89% increase in newly synthesized Etn lipids relative to controls (P < 0.05). Furthermore, the cerebellar PlsEtn/phosphatidylethanolamine ratio and molar percentage of PlsEtn were significantly elevated by 12% and 8%, respectively (P < 0.05). These data suggest that myo-Ins influences Etn lipid metabolism in brain, particularly in the cerebellum where there is a stimulation in the biosynthesis of new Etn lipids with a preference towards PlsEtn.

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“…In another study, it was observed [34] that high dietary fat for eight weeks decreased the PEA levels in the small intestine of mice, but not after 14 weeks of high-fat diet. To date, no data exists regarding the effect of dietary ethanolamine on PEA or other NAE tissue levels, although it has been seen that the contribution of an ethanolamine supplement increases the levels in the brain of phosphatidylethanolamine and also in liver microsomes [35,36]…”

Section: Diet Modify Pea Levelsmentioning

confidence: 99%

Therapeutic Efficacy of Palmitoylethanolamide and Its New Formulations in Synergy with Different Antioxidant Molecules Present in Diets

et al. 2019

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The use of a complete nutritional approach seems increasingly promising to combat chronic inflammation. The choice of healthy sources of carbohydrates, fats, and proteins, associated with regular physical activity and avoidance of smoking is essential to fight the war against chronic diseases. At the base of the analgesic, anti-inflammatory, or antioxidant action of the diets, there are numerous molecules, among which some of a lipidic nature very active in the inflammatory pathway. One class of molecules found in diets with anti-inflammatory actions are ALIAmides. Among all, one is particularly known for its ability to counteract the inflammatory cascade, the Palmitoylethanolamide (PEA). PEA is a molecular that is present in nature, in numerous foods, and is endogenously produced by our body, which acts as a balancer of inflammatory processes, also known as endocannabionoid-like. PEA is often used in the treatment of both acute and chronic inflammatory pathologies, either alone or in association with other molecules with properties, such as antioxidants or analgesics. This review aims to illustrate an overview of the different diets that are involved in the process of opposition to the inflammatory cascade, focusing on capacity of PEA and new formulations in synergy with other molecules.

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Effects of ethanolamine (ETN) Administration on etn and choline (CH) levels in plasma, brain extracellular fluid (ECF) and brain tissue, and on brain phospholipid levels in rats: An in vivo study

Cited by 12 publications

References 38 publications

Phospholipid biosynthetic enzymes in human brain

Phospholipid biosynthetic enzymes in human brain

Administration of Myo-inositol Plus Ethanolamine Elevates Phosphatidylethanolamine Plasmalogen in the Rat Cerebellum

Therapeutic Efficacy of Palmitoylethanolamide and Its New Formulations in Synergy with Different Antioxidant Molecules Present in Diets

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