Choline dietary requirement

In addition to the above water-soluble vitamins, other compounds are present in milk, such as choline, myo-inositol, and para-aminoben-zoic acid, compounds for which there is no proof of a dietary requirement for humans (NAS 1980A). 

Choline, supplied as dietary PC or as free choline, is required in the diet by rats. Although it has not been established that choline is required by humans, it is probably an essential nutrient and may, in the future, be classified as an essential amine or vitamin, Its possible requirement is a concern to clinicians feeding patients by total parenteral nutrition (TpN), In this type of feeding, which may be used for a year or longer, the patient is sustained intravenously with an artificial, chemically defined diet. The choline in foods occurs mainly as PC rather than as free choline. PC is a more desirable dietary component because, when free choline is consumed in large amounts, it is degraded by the gut bacteria to produce trimethylamine, an odoriferous compound (Magil et ai, 1981). 

Choline is a source of methyl groups for metabolic activity. It is not always grouped with the water-soluble B vitamins. It can be made in the body, but under some conditions it might become essential in the diet. In various species choline deficiency has been associated with fatty liver, cirrhosis, hemorrhagic kidney, and later development of a renal type of hypertension. The significance of these findings in man is not established, and there is, as yet, no clear therapeutic value of supplying choline in human diets, as distinct from other dietary improvement. Therefore any dietary requirement can not be estimated. 

SNPs (single nucleotide polymorphisms) in humans may exist and, if so, would influence dietary requirements for choline. In mice in which this gene is knocked out, the dietary requirement for choline is increased and they get fatty liver when eating a normal choline diet. Estrogen induces greater activity of PEMT perhaps explaining why premenopausal women require less choline in their diets. In addition to formation of choline, this enzyme has an essential role in lipoprotein secretion from the liver. 

That tissues are able to synthesize their own phospholipids could also be inferred from the fact that most of their constituents (choline is one exception) are not essential dietary requirements. However, in spite of the impetus given to biosynthetic studies by the tracer work in the 1930s and 1940s, the major treatise on phospholipids in the early 1950s (Wittcoff s Phosphatides) could give virtually no information about their biosynthesis. 

Equally, demonstrating that a compound has a physiological function as a coenzyme or hormone does not classify that compound as a vitamin. It is necessary to demonstrate that endogenous synthesis of the compound is inadequate to meet physiological requirements in the absence of a dietary source of the compound. Table 1.3 lists compounds that have clearly defined functions, but are not considered vitamins because they are not dietary essentials endogenous synthesis normally meets requirements. However, there is some evidence that premature infants and patients maintained on long-term total parenteral nutrition may be unable to meet their requirements for carnitine (Section 14.1.2), choline (Section 14.2.2), and taurine (Section 14.5.3) unless they are provided in the diet, and these are sometimes regarded as... 

In many animals, dietary deprivation of choline leads to liver dysfunction and growth retardation, and some patients maintained on choline-free total parenteral nutrition develop liver damage that resolves when choline is provided, suggesting that endogenous synthesis may be inadequate to meet requirements (Zeisel, 2000). There is inadequate information to permit the setting of reference intakes, but the Acceptable Intake for adults is 550 mg (for men) or 425 mg (for women) per day (Institute of Medicine, 1998). In experimental animals choline deficiency is exacerbated by deficiency of methionine, folic acid, or vitamin B12, which impairs the capacity for de novo synthesis. 

In recent years, pharmaceutical patents accounted for almost 25% of the nonfood patent activity. Pharmaceutical applications, particularly those involving liposomes, should require increasing quantities of refined lecithins. An increased demand for lecithin as a dietary supplement is also anticipated, as the result of dietary reference intakes being established for choline. Besides being a multifunctional food ingredient, lecithin has the benefit of being a widely recognized health food. 

Methionine, USP. An adequate diet should provide the methionine ncccs.sary for normal metabolism in the human.. Viethionine is considered an essential amino acid in humans. It is the precursor in the biosynthesis of -adcnosylnie(hio-niiic, which is an important methylating coenzyme involved In a variety of methylations (e.g.. N-me(hyla(ion of norepinephrine to form epinephrine and O-methylation of catecholamines catalyzed by ca(cchul-CI-mcthyl(iansfcra.ses). Adenosylmcthionine also participates in the methylation of pho.sphatidylcthanolaininc to form phosphatidylcholine, but this pathway is not efficient enough to provide all of the choline required hy higher animals hence, adequate dietary availability of choline is ncces.sary. ... 

CAS 62-49-7. (CH3)3N(OH)CH2CH2OH. Member of the vitamin B complex. Essential in the diet of rats, rabbits, chickens, and dogs. In humans it is required for lecithin formation and can replace methionine in the diet. There is no evidence of disease in humans caused by choline deficiency. It is a dietary factor important in furnishing free methyl groups for transmethylation has a lipotropic function. 

Lipotrophic factors are those required for transportation of triacylglycerol from the liver to the adipose tissue for storage. These factors are those that cannot be synthesized from nonlipotrophic components of the diet. The major role of lipotrophic factors is the formation of phosphatidylcholine, which is critical in VLDL formation. One of the lipotrophic factors obviously would be choline, which can be incorporated into phosphatidylcholine. Two other lipotrophic factors are related to the potential de novo synthesis of choline. The first and foremost is methionine, which can be used to donate the methyl groups for choline formation in the absence of dietary choline, thus allowing lipids to be moved from liver to adipose tissue (Fig. 18.7). 

Phosphatidylcholine is the major phospholipid on the surface monolayer of all lipoproteins, including VLDLs. In the liver, phosphatidylcholine is synthesized by two biosynthetic pathways the CDP-choline pathway and the phosphatidylethanolamine A -methyltransferase pathway (Chapter 8). Choline is an essential biosynthetic precursor of phosphatidylcholine via the CDP-choline pathway. When cells or animals are deprived of choline, plasma levels of TG and apo B are markedly reduced and TG accumulates in the liver, resulting in fatty liver. These observations led to the widely held view that the fatty liver caused by choline deficiency is due to inhibition of PC synthesis, which in turn would decrease VLDL secretion. This hypothesis was tested in primary rat hepatocytes cultured in medium lacking choline. Upon removal of choline/methionine from culture medium, the TG content of hepatocytes was increased 6-fold, and the secretion of TG and apo B in VLDL was markedly reduced. The interpretation of these experiments was that hepatic VLDL secretion requires the synthesis of phosphatidylcholine from either the CDP-choline or methylation pathways which require choline or methionine, respectively, as precursors (D.E. Vance, 1988). However, since choline deprivation was induced in a background of methionine insufficiency, it was not clear whether the lack of choline per se, and inhibition of the choline pathway for phosphatidylcholine synthesis, decreased VLDL secretion. More recent experiments have shown, surprisingly, that deficiency of choline in primary mouse hepatocytes does not reduce, but increases, phosphatidylcholine synthesis via the CDP-choline pathway, and does not decrease VLDL secretion (J.E. Vance, 2004). Thus, a deficiency of dietary choline reduces plasma TG and apo B levels by a mechanism that does not involve reduction of phosphatidylcholine synthesis. 

Neural membrane glycerophospholipids are synthesized from three dietary components polyunsaturated fatty acids, uridine monophosphate (UMP), and choline (Farooqui and Horrocks, 2007). Administration of above nutrients increases the level of glycerophospholipids, specific pre- or postsynaptic proteins, and the number of dendritic spines - a requirement for new synapse formation (Wurtman et al., 2009 Kamphnis and Wurtman, 2009). These effects are markedly enhanced when animals receive all three compounds together. This multi-nutrient approach in animals has also been shown to decrease A plaque burden, improve learning and memory through increased cholinergic neurotransmission, and have a neuroprotective effect in several mouse models of AD (Wurtman et al., 2009 ... 

Although AIs have been set for choline, there are few data to assess whether a dietary supply of choline is needed at all stages of the fife cycle, and it may be that the chofine requirement can be met by endogenous synthesis at some of these stages... 

Animals also derive methyl groups from dietary choline, which can partially substitute for the methionine nutritional requirement. An oxidation product of choline, betaine, is the actual methyl donor to homocysteine. This probably represents a salvage pathway for methyl groups in the catabolism of choline, but it can be of considerable importance if the capacity for de novo methyl synthesis is limited. 

Recommended dietary allowances for a male adult (daily intake, in foods and food supplements) of some nutrients, usually the amounts estimated as needed to prevent overt manifestation of deficiency disease in most persons. For the substances listed in smaller amounts the optimum intake, leading to the best of health, may be somewhat greater. Not shown, but probably or possibly required, are the essential fatty acids, />aminobenzoic acid, choline, vitamin D, vitamin K, chromium, manganese, cobalt, nickel, zinc, selenium, molybdenum, vanadium, tin, and silicon. 

The requirement for choline is influenced by the amounts of methionine, folacin, and vitamin B-12 in the diet, plus the growth rate of the individual, the energy intake and expenditure, the amount and type of dietary fat, the type of carEtohy-drate eaten, the total amount of protein in the diet, and possibly the amount of dietary cholesterol. As a result, the exact human requirement has not been established. 

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