Correlation of enzymatic, metabolic, and behavioral deficits in thiamin deficiency and its reversal
To clarify the enzymatic mechanisms of brain damage in thiamin deficiency, glucose oxidation, acetylcholine synthesis, and the activities of the three major thiamin pyrophosphate (TPP) dependent brain enzymes were compared in untreated controls, in symptomatic pyrithiamin-induced thiamin-deficient r...
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Veröffentlicht in: | Neurochemical research 1984-06, Vol.9 (6), p.803-814 |
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description | To clarify the enzymatic mechanisms of brain damage in thiamin deficiency, glucose oxidation, acetylcholine synthesis, and the activities of the three major thiamin pyrophosphate (TPP) dependent brain enzymes were compared in untreated controls, in symptomatic pyrithiamin-induced thiamin-deficient rats, and in animals in which the symptoms had been reversed by treatment with thiamin. Although brain slices from symptomatic animals produced 14CO2 and 14C-acetylcholine from [U-14C]glucose at rates similar to controls under resting conditions, their K+-induced-increase declined by 50 and 75%, respectively. In brain homogenates from these same animals, the activities of two TPP-dependent enzymes transketolase (EC 2.2.1.1) and 2-oxoglutarate dehydrogenase complex (EC 1.2.4.2, EC 2.3.1.61, EC 1.6.4.3) decreased 60-65% and 36%, respectively. The activity of the third TPP-dependent enzyme, pyruvate dehydrogenase complex (EC 1.2.4.1, EC 2.3.1.12, EC 1.6.4.3) did not change nor did the activity of its activator pyruvate dehydrogenase phosphate phosphatase (EC 3.1.3.43). Although treatment with thiamin for seven days reversed the neurological symptoms and restored glucose oxidation, acetylcholine synthesis and 2-oxoglutarate dehydrogenase activity to normal, transketolase activity remained 30-32% lower than controls. The activities of other TPP-independent enzymes (hexokinase, phosphofructokinase, and glutamate dehydrogenase) were normal in both deficient and reversed animals. |
doi_str_mv | 10.1007/bf00965667 |
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E ; KSIEZAK-REDING, H ; KWAN-FU REX SHEU ; MYKYTYN, V ; BLASS, J. P</creator><creatorcontrib>GIBSON, G. E ; KSIEZAK-REDING, H ; KWAN-FU REX SHEU ; MYKYTYN, V ; BLASS, J. P</creatorcontrib><description>To clarify the enzymatic mechanisms of brain damage in thiamin deficiency, glucose oxidation, acetylcholine synthesis, and the activities of the three major thiamin pyrophosphate (TPP) dependent brain enzymes were compared in untreated controls, in symptomatic pyrithiamin-induced thiamin-deficient rats, and in animals in which the symptoms had been reversed by treatment with thiamin. Although brain slices from symptomatic animals produced 14CO2 and 14C-acetylcholine from [U-14C]glucose at rates similar to controls under resting conditions, their K+-induced-increase declined by 50 and 75%, respectively. In brain homogenates from these same animals, the activities of two TPP-dependent enzymes transketolase (EC 2.2.1.1) and 2-oxoglutarate dehydrogenase complex (EC 1.2.4.2, EC 2.3.1.61, EC 1.6.4.3) decreased 60-65% and 36%, respectively. The activity of the third TPP-dependent enzyme, pyruvate dehydrogenase complex (EC 1.2.4.1, EC 2.3.1.12, EC 1.6.4.3) did not change nor did the activity of its activator pyruvate dehydrogenase phosphate phosphatase (EC 3.1.3.43). Although treatment with thiamin for seven days reversed the neurological symptoms and restored glucose oxidation, acetylcholine synthesis and 2-oxoglutarate dehydrogenase activity to normal, transketolase activity remained 30-32% lower than controls. The activities of other TPP-independent enzymes (hexokinase, phosphofructokinase, and glutamate dehydrogenase) were normal in both deficient and reversed animals.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/bf00965667</identifier><identifier>PMID: 6149477</identifier><identifier>CODEN: NEREDZ</identifier><language>eng</language><publisher>New York, NY: Springer</publisher><subject>Animals ; Biological and medical sciences ; Brain - enzymology ; Brain - metabolism ; Hexokinase - metabolism ; Ketoglutarate Dehydrogenase Complex - metabolism ; Male ; Medical sciences ; Metabolic diseases ; Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...) ; Pyruvate Dehydrogenase Complex - metabolism ; Rats ; Rats, Inbred Strains ; Thiamine Deficiency - enzymology ; Thiamine Deficiency - metabolism ; Thiamine Pyrophosphatase - metabolism ; Transketolase - metabolism</subject><ispartof>Neurochemical research, 1984-06, Vol.9 (6), p.803-814</ispartof><rights>1985 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-2b76d311d383caf71591d50a8dfd7f0009f969555728d2eb2b9dfd46b741b6923</citedby><cites>FETCH-LOGICAL-c408t-2b76d311d383caf71591d50a8dfd7f0009f969555728d2eb2b9dfd46b741b6923</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27911,27912</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=9093588$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6149477$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GIBSON, G. E</creatorcontrib><creatorcontrib>KSIEZAK-REDING, H</creatorcontrib><creatorcontrib>KWAN-FU REX SHEU</creatorcontrib><creatorcontrib>MYKYTYN, V</creatorcontrib><creatorcontrib>BLASS, J. P</creatorcontrib><title>Correlation of enzymatic, metabolic, and behavioral deficits in thiamin deficiency and its reversal</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><description>To clarify the enzymatic mechanisms of brain damage in thiamin deficiency, glucose oxidation, acetylcholine synthesis, and the activities of the three major thiamin pyrophosphate (TPP) dependent brain enzymes were compared in untreated controls, in symptomatic pyrithiamin-induced thiamin-deficient rats, and in animals in which the symptoms had been reversed by treatment with thiamin. Although brain slices from symptomatic animals produced 14CO2 and 14C-acetylcholine from [U-14C]glucose at rates similar to controls under resting conditions, their K+-induced-increase declined by 50 and 75%, respectively. In brain homogenates from these same animals, the activities of two TPP-dependent enzymes transketolase (EC 2.2.1.1) and 2-oxoglutarate dehydrogenase complex (EC 1.2.4.2, EC 2.3.1.61, EC 1.6.4.3) decreased 60-65% and 36%, respectively. The activity of the third TPP-dependent enzyme, pyruvate dehydrogenase complex (EC 1.2.4.1, EC 2.3.1.12, EC 1.6.4.3) did not change nor did the activity of its activator pyruvate dehydrogenase phosphate phosphatase (EC 3.1.3.43). Although treatment with thiamin for seven days reversed the neurological symptoms and restored glucose oxidation, acetylcholine synthesis and 2-oxoglutarate dehydrogenase activity to normal, transketolase activity remained 30-32% lower than controls. The activities of other TPP-independent enzymes (hexokinase, phosphofructokinase, and glutamate dehydrogenase) were normal in both deficient and reversed animals.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain - enzymology</subject><subject>Brain - metabolism</subject><subject>Hexokinase - metabolism</subject><subject>Ketoglutarate Dehydrogenase Complex - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...)</subject><subject>Pyruvate Dehydrogenase Complex - metabolism</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Thiamine Deficiency - enzymology</subject><subject>Thiamine Deficiency - metabolism</subject><subject>Thiamine Pyrophosphatase - metabolism</subject><subject>Transketolase - metabolism</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1984</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM1LAzEQxYMotVYv3oU9iAdxNdlsks1Ri1Wh4EXPSz5pJLvRZFuof72prb16ejPzfjyYB8A5grcIQnYnLYScEkrZARgjwnBJOcSHYAwxrUuMODwGJyl9QJjxCo3AiKKa14yNgZqGGI0Xgwt9EWxh-u91lzd1U3RmEDL4zSh6XUizECsXovCFNtYpN6TC9cWwcKLLur2ZXq1_6Y0bzcrEJPwpOLLCJ3O20wl4nz2-TZ_L-evTy_R-XqoaNkNZSUY1RkjjBithGSIcaQJFo61m-UPILaecEMKqRldGVpJnp6aS1UhSXuEJuNrmfsbwtTRpaDuXlPFe9CYsU9sgDCmp8L8gwrxGDNMMXm9BFUNK0dj2M7pOxHWLYLupvn2Y_VWf4Ytd6lJ2Ru_RXdfZv9z5IinhbRS9cmmPccgxaRr8AwdHitY</recordid><startdate>198406</startdate><enddate>198406</enddate><creator>GIBSON, G. 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P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-2b76d311d383caf71591d50a8dfd7f0009f969555728d2eb2b9dfd46b741b6923</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1984</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brain - enzymology</topic><topic>Brain - metabolism</topic><topic>Hexokinase - metabolism</topic><topic>Ketoglutarate Dehydrogenase Complex - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...)</topic><topic>Pyruvate Dehydrogenase Complex - metabolism</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Thiamine Deficiency - enzymology</topic><topic>Thiamine Deficiency - metabolism</topic><topic>Thiamine Pyrophosphatase - metabolism</topic><topic>Transketolase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GIBSON, G. E</creatorcontrib><creatorcontrib>KSIEZAK-REDING, H</creatorcontrib><creatorcontrib>KWAN-FU REX SHEU</creatorcontrib><creatorcontrib>MYKYTYN, V</creatorcontrib><creatorcontrib>BLASS, J. P</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>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GIBSON, G. E</au><au>KSIEZAK-REDING, H</au><au>KWAN-FU REX SHEU</au><au>MYKYTYN, V</au><au>BLASS, J. P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Correlation of enzymatic, metabolic, and behavioral deficits in thiamin deficiency and its reversal</atitle><jtitle>Neurochemical research</jtitle><addtitle>Neurochem Res</addtitle><date>1984-06</date><risdate>1984</risdate><volume>9</volume><issue>6</issue><spage>803</spage><epage>814</epage><pages>803-814</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><coden>NEREDZ</coden><abstract>To clarify the enzymatic mechanisms of brain damage in thiamin deficiency, glucose oxidation, acetylcholine synthesis, and the activities of the three major thiamin pyrophosphate (TPP) dependent brain enzymes were compared in untreated controls, in symptomatic pyrithiamin-induced thiamin-deficient rats, and in animals in which the symptoms had been reversed by treatment with thiamin. Although brain slices from symptomatic animals produced 14CO2 and 14C-acetylcholine from [U-14C]glucose at rates similar to controls under resting conditions, their K+-induced-increase declined by 50 and 75%, respectively. In brain homogenates from these same animals, the activities of two TPP-dependent enzymes transketolase (EC 2.2.1.1) and 2-oxoglutarate dehydrogenase complex (EC 1.2.4.2, EC 2.3.1.61, EC 1.6.4.3) decreased 60-65% and 36%, respectively. The activity of the third TPP-dependent enzyme, pyruvate dehydrogenase complex (EC 1.2.4.1, EC 2.3.1.12, EC 1.6.4.3) did not change nor did the activity of its activator pyruvate dehydrogenase phosphate phosphatase (EC 3.1.3.43). Although treatment with thiamin for seven days reversed the neurological symptoms and restored glucose oxidation, acetylcholine synthesis and 2-oxoglutarate dehydrogenase activity to normal, transketolase activity remained 30-32% lower than controls. The activities of other TPP-independent enzymes (hexokinase, phosphofructokinase, and glutamate dehydrogenase) were normal in both deficient and reversed animals.</abstract><cop>New York, NY</cop><pub>Springer</pub><pmid>6149477</pmid><doi>10.1007/bf00965667</doi><tpages>12</tpages></addata></record> |
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subjects | Animals Biological and medical sciences Brain - enzymology Brain - metabolism Hexokinase - metabolism Ketoglutarate Dehydrogenase Complex - metabolism Male Medical sciences Metabolic diseases Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...) Pyruvate Dehydrogenase Complex - metabolism Rats Rats, Inbred Strains Thiamine Deficiency - enzymology Thiamine Deficiency - metabolism Thiamine Pyrophosphatase - metabolism Transketolase - metabolism |
title | Correlation of enzymatic, metabolic, and behavioral deficits in thiamin deficiency and its reversal |
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