Liver Microsomal Phosphatidyl Choline Biosynthesis in Choline Deficiency

Skurdal, David N.; Cornatzer, W. E.

doi:10.3181/00379727-145-37940

Cited by 9 publications

(4 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The enzyme catalysing these reactions, phosphatidylethanolamine Nmethyltransferase (EC 2.1.1.17), uses AdoMet as the methyl donor [35,36], and choline deficiency does increase the utilization of AdoMet for phosphatidylcholine synthesis [33,37,38]. This depletes limited stores of AdoMet in the liver, which in turn acts to limit the amount of phosphatidylcholine that can be formed by this pathway during choline deficiency [39,40]. We observed accumulation of AdoHcy, suggesting that the rate of AdoHcy formation (AdoMet utilization) was increased relative to the rate of AdoHcy hydrolysis.…”

Section: Discussionmentioning

confidence: 99%

Effect of choline deficiency on S-adenosylmethionine and methionine concentrations in rat liver

Zeisel

Zola

daCosta

et al. 1989

Biochemical Journal

101

View full text Add to dashboard Cite

Choline and C1 metabolism pathways intersect at the formation of methionine from homocysteine. Hepatic S-adenosylmethionine (AdoMet) concentrations are decreased in animals ingesting diets deficient in choline, and it has been suggested that this occurs because the availability of methionine limits AdoMet synthesis. If the above hypothesis is correct, changes in hepatic AdoMet concentrations should relate in some consistent manner to changes in hepatic methionine concentrations. Rats were fed on a choline-deficient or control diet for 1-42 days. Hepatic choline concentrations in control animals were 105 nmol/g, and decreased to 50% of control after the first 7 days on the choline-deficient diet. Hepatic methionine concentrations decreased by less than 20%, with most of this decrease occurring between days 3 and 7 of choline deficiency. Hepatic AdoMet concentrations decreased by 25% during the first week, and continued to decrease (in total, by over 60%) during each subsequent week during which animals consumed a choline-deficient diet. Hepatic S-adenosylhomocysteine (AdoHcy) concentrations increased by 50% when animals consumed a choline-deficient diet. AdoHcy is formed when AdoMet is utilized as a methyl donor. In summary, choline deficiency can deplete hepatic stores of AdoMet under dietary conditions that only minimally decrease the availability of methionine within liver. Thus decreased availability of methionine may not have been the only mechanism whereby choline deficiency lowers hepatic AdoMet concentrations. We suggest that increased utilization of AdoMet might also have occurred.

show abstract

Section: Discussionmentioning

confidence: 99%

Effect of choline deficiency on S-adenosylmethionine and methionine concentrations in rat liver

Zeisel

Zola

daCosta

et al. 1989

Biochemical Journal

101

View full text Add to dashboard Cite

show abstract

“…In hepatocytes exogenous albumin-bound fatty acids greatly stimulate triacylglycerol synthesis, but show smaller effects on phospholipid formation (Ontko, 1972;Sundler et at., 1974a), indicating the existence of metabolic control at this point. Several control points and mechanisms must be considered: (1) the activities and relative affinities for diacylglycerol of cholinephosphotransferase, ethanolaminephosphotransferase and diacylglycerol acyltransferase (Young &Lynen, 1969 ;Skurdal & Cornatzer, 1974;Fallon et al, 1975;Sribney et al, 1976;Kanoh & Ohno, 1976); (2) the influence on diacylglycerol utilization by its fatty acid structure (Hill et al, 1968;Kanoh, 1969;Akesson et al, 1970;D e KruyfT et al, 1970;Sundler et al, 1974a;Kanoh & Ohno, 1975 ;Fallon et al, 1976); (3) the effects on phosphotransferase activities by the concentrations of CDP bases (Sundler & Akesson, 19756) regulated ( 3 4 at the cytidylyltransferase steps (Fiscus & Schneider, 1966;Sundler & Akesson, 19756;Sundler, 1975), (36) at the kinase steps (Weinhold & Rethy, 1974) and/or (3c) by the supply of free bases (Sundler & Akesson, 19756).…”

Section: Fig 1 Rates Of Transport In Phosphoglyceride Biosynthesis mentioning

confidence: 99%

Factors Controlling the Biosynthesis of Individual Phosphoglycerides in Liver

Åkesson

Sundler

1977

Biochemical Society Transactions

View full text Add to dashboard Cite

(2) The redirection of phosphatidate utilization probably partly explains the phospholipidosis which is observed after prolonged treatment with high doses of many cationic drugs. The drugs stimulate the synthesis of acidic lipids which are subsequently transported to the lysosomes with the drugs. The situation is probably aggravated further by an inability of the lysosomes to degrade this abnormal substrate (Michell et al., 1976). (3) The cationic drugs which have been discussed generally interfere with membranelinked phenomena, such as movement, fusion, permeability, transport and receptor function (Brindley er al., 1975). Although these processes are not well understood, the turnover of acidic phospholipids seems to be involved. Cationic drugs have been shown to interfere with this turnover and to control the pattern of phospholipid which is synthesized. This in turn could contribute to the observed changes in membrane properties. Foundation and Servier Laboratories Ltd. for financial assistance.

show abstract

“…In a similar manner, it is disputed througl~out the literature as to whether methylation sf PtdEtn increases (41,6,(14)(15)(16)(17)(18)(19)(20)(21)(22) or decreases (3,7,13,(23)(24)(25)(26)(27) during choline deficiency. Specifically, a significant increase in PtdEtn methylation during choline and (or) methisnine deficiency is consistently observed by in vitro analysis (4,14,15,(20)(21)(22) ; however, incorporation of [methyl-14C]methionine (1 3, 17-20, 26, 271, [ I T ] -ethanslamine (23-25), or 13,16,17) has resulted in conflicting interpretations.…”

mentioning

confidence: 93%

Effects of a methyl-deficient diet on rat liver phosphatidylcholine biosynthesis

Hoffman¹,

Haning²,

Cornatzer³

1981

Can. J. Biochem.

Self Cite

View full text Add to dashboard Cite

To produce a severe choline-methionine deficiency, a synthetic L-amino acid diet, free of choline, methionine, vitamin B12, and folic acid and supplemented with guanidoacetic acid, a methyl group acceptor, was fed to female rats for 2 weeks. The in vitro activity of liver microsomal phosphatidylethanolamine methyltransferase was stimulated twofold when compared with basal diet controls. The activity of choline phosphotransferase was depressed by 86%; thus, the contribution of the methyltransferase in the overall synthesis of phosphatidylcholine apparently increased. However, measurement of the in vivo methylation of phosphatidylethanolamine by incorporation of [1,2-14C]ethanolamine into phosphatidylcholine indicates that the methylation pathway is markedly depressed in methyl deficiency. Hepatic concentrations of the methyltransferase substrate, S-adenosylmethionine, and the inhibitory metabolite, S-adenosylhomocysteine, were significantly altered such that an unfavorable environment for methylation was present in the deficient animal. The ratio of substrate to inhibitor was depressed from 5.2:1 in the controls to 1.7:1 in the livers of methyl-depleted rats. Control of transmethylation in accordance with the availability of substrates, phosphatidylethanolamine, or S-adenosylmethionine, and the level of S-adenosylhomocysteine is discussed.

show abstract

Liver Microsomal Phosphatidyl Choline Biosynthesis in Choline Deficiency

Cited by 9 publications

References 8 publications

Effect of choline deficiency on S-adenosylmethionine and methionine concentrations in rat liver

Effect of choline deficiency on S-adenosylmethionine and methionine concentrations in rat liver

Factors Controlling the Biosynthesis of Individual Phosphoglycerides in Liver

Effects of a methyl-deficient diet on rat liver phosphatidylcholine biosynthesis

Contact Info

Product

Resources

About