Free Acetate Production by Rat Hepatocytes during Peroxisomal Fatty Acid and Dicarboxylic Acid Oxidation
The fate of the acetyl-CoA units released during peroxisomal fatty acid oxidation was studied in isolated hepatocytes from normal and peroxisome-proliferated rats. Ketogenesis and hydrogen peroxide generation were employed as indicators of mitochondrial and peroxisomal fatty acid oxidation, respecti...
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| Veröffentlicht in: | The Journal of biological chemistry 1989-06, Vol.264 (18), p.10347-10350 |
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| creator | Leighton, F Bergseth, S Rørtveit, T Christiansen, E N Bremer, J |
| description | The fate of the acetyl-CoA units released during peroxisomal fatty acid oxidation was studied in isolated hepatocytes from normal and peroxisome-proliferated rats. Ketogenesis and hydrogen peroxide generation were employed as indicators of mitochondrial and peroxisomal fatty acid oxidation, respectively. Butyric and hexanoic acids were employed as mitochondrial substrates, 1,ω-dicarboxylic acids as predominantly peroxisomal substrates, and lauric acid as a substrate for both mitochondria and peroxisomes. Ketogenesis from dicarboxylic acids was either absent or very low in normal and peroxisome-proliferated hepatocytes, but free acetate release was detected at rates that could account for all the acetyl-CoA produced in peroxisomes by dicarboxylic and also by monocarboxylic acids. Mitochondrial fatty acid oxidation also led to free acetate generation but at low rates relative to ketogenesis. The origin of the acetate released was confirmed employing [1-14C]dodecanedioic acid. Thus, the activity of peroxisomes might contribute significantly to the free acetate generation known to occur during fatty acid oxidation in rats and possibly also in humans. |
| doi_str_mv | 10.1016/S0021-9258(18)81625-8 |
| format | Article |
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Ketogenesis and hydrogen peroxide generation were employed as indicators of mitochondrial and peroxisomal fatty acid oxidation, respectively. Butyric and hexanoic acids were employed as mitochondrial substrates, 1,ω-dicarboxylic acids as predominantly peroxisomal substrates, and lauric acid as a substrate for both mitochondria and peroxisomes. Ketogenesis from dicarboxylic acids was either absent or very low in normal and peroxisome-proliferated hepatocytes, but free acetate release was detected at rates that could account for all the acetyl-CoA produced in peroxisomes by dicarboxylic and also by monocarboxylic acids. Mitochondrial fatty acid oxidation also led to free acetate generation but at low rates relative to ketogenesis. The origin of the acetate released was confirmed employing [1-14C]dodecanedioic acid. Thus, the activity of peroxisomes might contribute significantly to the free acetate generation known to occur during fatty acid oxidation in rats and possibly also in humans.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1016/S0021-9258(18)81625-8</identifier><identifier>PMID: 2732225</identifier><identifier>CODEN: JBCHA3</identifier><language>eng</language><publisher>Bethesda, MD: Elsevier Inc</publisher><subject>Acetates - metabolism ; acetic acid ; Animals ; Bezafibrate - pharmacology ; Biological and medical sciences ; Cells, Cultured ; dicarboxylic acids ; Dicarboxylic Acids - metabolism ; Fatty Acids - metabolism ; Fundamental and applied biological sciences. Psychology ; Hydrogen Peroxide - metabolism ; Ketone Bodies - metabolism ; Kinetics ; Liver - drug effects ; Liver - metabolism ; Liver. Bile. Biliary tracts ; Male ; Microbodies - drug effects ; Microbodies - metabolism ; Oxidation-Reduction ; peroxisomes ; Rats ; Rats, Inbred Strains ; Vertebrates: digestive system</subject><ispartof>The Journal of biological chemistry, 1989-06, Vol.264 (18), p.10347-10350</ispartof><rights>1989 © 1989 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology.</rights><rights>1991 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c549t-ddb50f6721e987bb0c5b13d95ebe644d0c611f3fd8a91a66e0641a0bb8e8529a3</citedby><cites>FETCH-LOGICAL-c549t-ddb50f6721e987bb0c5b13d95ebe644d0c611f3fd8a91a66e0641a0bb8e8529a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19420037$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2732225$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Leighton, F</creatorcontrib><creatorcontrib>Bergseth, S</creatorcontrib><creatorcontrib>Rørtveit, T</creatorcontrib><creatorcontrib>Christiansen, E N</creatorcontrib><creatorcontrib>Bremer, J</creatorcontrib><title>Free Acetate Production by Rat Hepatocytes during Peroxisomal Fatty Acid and Dicarboxylic Acid Oxidation</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>The fate of the acetyl-CoA units released during peroxisomal fatty acid oxidation was studied in isolated hepatocytes from normal and peroxisome-proliferated rats. Ketogenesis and hydrogen peroxide generation were employed as indicators of mitochondrial and peroxisomal fatty acid oxidation, respectively. Butyric and hexanoic acids were employed as mitochondrial substrates, 1,ω-dicarboxylic acids as predominantly peroxisomal substrates, and lauric acid as a substrate for both mitochondria and peroxisomes. Ketogenesis from dicarboxylic acids was either absent or very low in normal and peroxisome-proliferated hepatocytes, but free acetate release was detected at rates that could account for all the acetyl-CoA produced in peroxisomes by dicarboxylic and also by monocarboxylic acids. Mitochondrial fatty acid oxidation also led to free acetate generation but at low rates relative to ketogenesis. The origin of the acetate released was confirmed employing [1-14C]dodecanedioic acid. Thus, the activity of peroxisomes might contribute significantly to the free acetate generation known to occur during fatty acid oxidation in rats and possibly also in humans.</description><subject>Acetates - metabolism</subject><subject>acetic acid</subject><subject>Animals</subject><subject>Bezafibrate - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cells, Cultured</subject><subject>dicarboxylic acids</subject><subject>Dicarboxylic Acids - metabolism</subject><subject>Fatty Acids - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hydrogen Peroxide - metabolism</subject><subject>Ketone Bodies - metabolism</subject><subject>Kinetics</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Liver. Bile. Biliary tracts</subject><subject>Male</subject><subject>Microbodies - drug effects</subject><subject>Microbodies - metabolism</subject><subject>Oxidation-Reduction</subject><subject>peroxisomes</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Vertebrates: digestive system</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1989</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtv1DAURi0EKkPhJ1TyAhAsAn7EHmeFqsJQpEqteEjsLD9uOkaZeGo7MPn3JM2oLPHGku_5vmsdhM4oeUcJle-_EcJo1TCh3lD1VlHJRKUeoRUlildc0J-P0eoBeYqe5fyLTKdu6Ak6YWvOGBMrtN0kAHzuoJgC-CZFP7gSYo_tiL-agi9hb0p0Y4GM_ZBCf4tvIMVDyHFnOrwxpYxTPHhseo8_BmeSjYexC255vT4Eb-bC5-hJa7oML473Kfqx-fT94rK6uv785eL8qnKibkrlvRWklWtGoVFra4kTlnLfCLAg69oTJylteeuVaaiREoisqSHWKlCCNYafotdL7z7FuwFy0buQHXSd6SEOWVPBZcNrMYFiAV2KOSdo9T6FnUmjpkTPhvW9YT3r01Tpe8NaTbmz44LB7sA_pI5Kp_mr49xkZ7o2md6F_K-8qRkhfD1xLxduG263f0ICbUN0W9hpJut5ISW8nrEPCwaTtN8Bks4uQO_ATxFXtI_hPx_-C6I0pDk</recordid><startdate>19890625</startdate><enddate>19890625</enddate><creator>Leighton, F</creator><creator>Bergseth, S</creator><creator>Rørtveit, T</creator><creator>Christiansen, E N</creator><creator>Bremer, J</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>FR3</scope><scope>M7Z</scope><scope>P64</scope></search><sort><creationdate>19890625</creationdate><title>Free Acetate Production by Rat Hepatocytes during Peroxisomal Fatty Acid and Dicarboxylic Acid Oxidation</title><author>Leighton, F ; Bergseth, S ; Rørtveit, T ; Christiansen, E N ; Bremer, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c549t-ddb50f6721e987bb0c5b13d95ebe644d0c611f3fd8a91a66e0641a0bb8e8529a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1989</creationdate><topic>Acetates - metabolism</topic><topic>acetic acid</topic><topic>Animals</topic><topic>Bezafibrate - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cells, Cultured</topic><topic>dicarboxylic acids</topic><topic>Dicarboxylic Acids - metabolism</topic><topic>Fatty Acids - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hydrogen Peroxide - metabolism</topic><topic>Ketone Bodies - metabolism</topic><topic>Kinetics</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>Liver. Bile. Biliary tracts</topic><topic>Male</topic><topic>Microbodies - drug effects</topic><topic>Microbodies - metabolism</topic><topic>Oxidation-Reduction</topic><topic>peroxisomes</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Vertebrates: digestive system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Leighton, F</creatorcontrib><creatorcontrib>Bergseth, S</creatorcontrib><creatorcontrib>Rørtveit, T</creatorcontrib><creatorcontrib>Christiansen, E N</creatorcontrib><creatorcontrib>Bremer, J</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biochemistry Abstracts 1</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Leighton, F</au><au>Bergseth, S</au><au>Rørtveit, T</au><au>Christiansen, E N</au><au>Bremer, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Free Acetate Production by Rat Hepatocytes during Peroxisomal Fatty Acid and Dicarboxylic Acid Oxidation</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>1989-06-25</date><risdate>1989</risdate><volume>264</volume><issue>18</issue><spage>10347</spage><epage>10350</epage><pages>10347-10350</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><coden>JBCHA3</coden><abstract>The fate of the acetyl-CoA units released during peroxisomal fatty acid oxidation was studied in isolated hepatocytes from normal and peroxisome-proliferated rats. Ketogenesis and hydrogen peroxide generation were employed as indicators of mitochondrial and peroxisomal fatty acid oxidation, respectively. Butyric and hexanoic acids were employed as mitochondrial substrates, 1,ω-dicarboxylic acids as predominantly peroxisomal substrates, and lauric acid as a substrate for both mitochondria and peroxisomes. Ketogenesis from dicarboxylic acids was either absent or very low in normal and peroxisome-proliferated hepatocytes, but free acetate release was detected at rates that could account for all the acetyl-CoA produced in peroxisomes by dicarboxylic and also by monocarboxylic acids. Mitochondrial fatty acid oxidation also led to free acetate generation but at low rates relative to ketogenesis. The origin of the acetate released was confirmed employing [1-14C]dodecanedioic acid. Thus, the activity of peroxisomes might contribute significantly to the free acetate generation known to occur during fatty acid oxidation in rats and possibly also in humans.</abstract><cop>Bethesda, MD</cop><pub>Elsevier Inc</pub><pmid>2732225</pmid><doi>10.1016/S0021-9258(18)81625-8</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of biological chemistry, 1989-06, Vol.264 (18), p.10347-10350 |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Acetates - metabolism acetic acid Animals Bezafibrate - pharmacology Biological and medical sciences Cells, Cultured dicarboxylic acids Dicarboxylic Acids - metabolism Fatty Acids - metabolism Fundamental and applied biological sciences. Psychology Hydrogen Peroxide - metabolism Ketone Bodies - metabolism Kinetics Liver - drug effects Liver - metabolism Liver. Bile. Biliary tracts Male Microbodies - drug effects Microbodies - metabolism Oxidation-Reduction peroxisomes Rats Rats, Inbred Strains Vertebrates: digestive system |
| title | Free Acetate Production by Rat Hepatocytes during Peroxisomal Fatty Acid and Dicarboxylic Acid Oxidation |
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