Alteration in the Phosphatidylcholine Biosynthesis of Rat Liver Microsomes Caused by Vitamin B6 Deficiency

Rats fed with a vitamin B 6 -deficient 70% casein diet for 5 weeks were found to have decreased considerably in the content of phosphatidylcholine (PC) in liver microsomes, presumably because of the depressed PC biosynthesis from choline or phosphatidylethanolamine (PE). The activities of choline ph...

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Veröffentlicht in:Bioscience, biotechnology, and biochemistry biotechnology, and biochemistry, 1995, Vol.59 (2), p.163-167
Hauptverfasser: She, Qing-Bai, Hayakawa, Takashi, Tsuge, Haruhito
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Hayakawa, Takashi
Tsuge, Haruhito
description Rats fed with a vitamin B 6 -deficient 70% casein diet for 5 weeks were found to have decreased considerably in the content of phosphatidylcholine (PC) in liver microsomes, presumably because of the depressed PC biosynthesis from choline or phosphatidylethanolamine (PE). The activities of choline phosphokinase and choline phosphotransferase in liver decreased, apparently, as compared with the pair-fed control or control rats. The hepatic level of the PE methyltransferase co-substrate, S-adenosylmethionine (SAM), decreased about 1/3, but the level of the inhibitory metabolite, S-adenosylhomocysteine (SAH), was elevated due to the marked reduction in the activities of cystathionine β-synthase and γ-cystathionase. The resultant molar ratio of SAM/SAH decreased drastically such that the methylation of PE to PC was decreased in vivo, as confirmed by lowering the activity of PE methyltransferase in vitro in response to a decreased molar ratio of SAM/SAH. A similar effect on the PE methylation was also observed in the pair-fed control rats, but the PC biosynthesis from choline clearly compensated for the drop of PC biosynthesis from PE. Results of this study demonstrate that vitamin B 6 deficiency modified methionine metabolism and decreased choline utilization, and thus indirectly affected the biosynthesis of PC in liver microsomes.
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The activities of choline phosphokinase and choline phosphotransferase in liver decreased, apparently, as compared with the pair-fed control or control rats. The hepatic level of the PE methyltransferase co-substrate, S-adenosylmethionine (SAM), decreased about 1/3, but the level of the inhibitory metabolite, S-adenosylhomocysteine (SAH), was elevated due to the marked reduction in the activities of cystathionine β-synthase and γ-cystathionase. The resultant molar ratio of SAM/SAH decreased drastically such that the methylation of PE to PC was decreased in vivo, as confirmed by lowering the activity of PE methyltransferase in vitro in response to a decreased molar ratio of SAM/SAH. A similar effect on the PE methylation was also observed in the pair-fed control rats, but the PC biosynthesis from choline clearly compensated for the drop of PC biosynthesis from PE. 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The activities of choline phosphokinase and choline phosphotransferase in liver decreased, apparently, as compared with the pair-fed control or control rats. The hepatic level of the PE methyltransferase co-substrate, S-adenosylmethionine (SAM), decreased about 1/3, but the level of the inhibitory metabolite, S-adenosylhomocysteine (SAH), was elevated due to the marked reduction in the activities of cystathionine β-synthase and γ-cystathionase. The resultant molar ratio of SAM/SAH decreased drastically such that the methylation of PE to PC was decreased in vivo, as confirmed by lowering the activity of PE methyltransferase in vitro in response to a decreased molar ratio of SAM/SAH. A similar effect on the PE methylation was also observed in the pair-fed control rats, but the PC biosynthesis from choline clearly compensated for the drop of PC biosynthesis from PE. 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Francis</general><general>Japan Society for Bioscience Biotechnology and Agrochemistry</general><general>Oxford University Press</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>1995</creationdate><title>Alteration in the Phosphatidylcholine Biosynthesis of Rat Liver Microsomes Caused by Vitamin B6 Deficiency</title><author>She, Qing-Bai ; Hayakawa, Takashi ; Tsuge, Haruhito</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i327t-f97e417e2becb82ab3f6f066ccc597afb68c17cf94b9eebb23cadb51f67dce403</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biotechnology</topic><topic>Caseins - administration &amp; dosage</topic><topic>Choline - metabolism</topic><topic>Choline Kinase - metabolism</topic><topic>Cystathionine beta-Synthase - metabolism</topic><topic>Cystathionine gamma-Lyase - metabolism</topic><topic>Diacylglycerol Cholinephosphotransferase - metabolism</topic><topic>Liver - drug effects</topic><topic>Liver - enzymology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Methylation</topic><topic>Methyltransferases - metabolism</topic><topic>Microsomes, Liver - enzymology</topic><topic>Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...)</topic><topic>Phosphatidylcholines - biosynthesis</topic><topic>Phosphatidylethanolamine N-Methyltransferase</topic><topic>Phosphatidylethanolamines - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>S-Adenosylhomocysteine - metabolism</topic><topic>S-Adenosylmethionine - metabolism</topic><topic>Vitamin B 6 Deficiency - enzymology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>She, Qing-Bai</creatorcontrib><creatorcontrib>Hayakawa, Takashi</creatorcontrib><creatorcontrib>Tsuge, Haruhito</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Bioscience, biotechnology, and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>She, Qing-Bai</au><au>Hayakawa, Takashi</au><au>Tsuge, Haruhito</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alteration in the Phosphatidylcholine Biosynthesis of Rat Liver Microsomes Caused by Vitamin B6 Deficiency</atitle><jtitle>Bioscience, biotechnology, and biochemistry</jtitle><addtitle>Biosci Biotechnol Biochem</addtitle><date>1995</date><risdate>1995</risdate><volume>59</volume><issue>2</issue><spage>163</spage><epage>167</epage><pages>163-167</pages><issn>0916-8451</issn><eissn>1347-6947</eissn><abstract>Rats fed with a vitamin B 6 -deficient 70% casein diet for 5 weeks were found to have decreased considerably in the content of phosphatidylcholine (PC) in liver microsomes, presumably because of the depressed PC biosynthesis from choline or phosphatidylethanolamine (PE). The activities of choline phosphokinase and choline phosphotransferase in liver decreased, apparently, as compared with the pair-fed control or control rats. The hepatic level of the PE methyltransferase co-substrate, S-adenosylmethionine (SAM), decreased about 1/3, but the level of the inhibitory metabolite, S-adenosylhomocysteine (SAH), was elevated due to the marked reduction in the activities of cystathionine β-synthase and γ-cystathionase. The resultant molar ratio of SAM/SAH decreased drastically such that the methylation of PE to PC was decreased in vivo, as confirmed by lowering the activity of PE methyltransferase in vitro in response to a decreased molar ratio of SAM/SAH. A similar effect on the PE methylation was also observed in the pair-fed control rats, but the PC biosynthesis from choline clearly compensated for the drop of PC biosynthesis from PE. Results of this study demonstrate that vitamin B 6 deficiency modified methionine metabolism and decreased choline utilization, and thus indirectly affected the biosynthesis of PC in liver microsomes.</abstract><cop>Tokyo</cop><pub>Taylor &amp; Francis</pub><pmid>7766014</pmid><doi>10.1271/bbb.59.163</doi><tpages>5</tpages></addata></record>
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subjects Animals
Biological and medical sciences
Biotechnology
Caseins - administration & dosage
Choline - metabolism
Choline Kinase - metabolism
Cystathionine beta-Synthase - metabolism
Cystathionine gamma-Lyase - metabolism
Diacylglycerol Cholinephosphotransferase - metabolism
Liver - drug effects
Liver - enzymology
Male
Medical sciences
Metabolic diseases
Methylation
Methyltransferases - metabolism
Microsomes, Liver - enzymology
Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...)
Phosphatidylcholines - biosynthesis
Phosphatidylethanolamine N-Methyltransferase
Phosphatidylethanolamines - metabolism
Rats
Rats, Wistar
S-Adenosylhomocysteine - metabolism
S-Adenosylmethionine - metabolism
Vitamin B 6 Deficiency - enzymology
title Alteration in the Phosphatidylcholine Biosynthesis of Rat Liver Microsomes Caused by Vitamin B6 Deficiency
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