Malonyl-CoA and long chain acyl-CoA esters as metabolic coupling factors in nutrient-induced insulin secretion
Several approaches were used to test the hypothesis proposing a role for acyl-CoA esters in nutrient-induced insulin release (Prentki, M., and Matschinsky, F. M. (1987) Physiol. Rev. 67, 1185-1248; Corkey, B. E., Glennon, M. C., Chen, K. S., Deeney, J. T., Matschinsky, F. M., and Prentki, M. (1989)...
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| Veröffentlicht in: | The Journal of biological chemistry 1992-03, Vol.267 (9), p.5802-5810 |
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| creator | PRENTKI, M VISCHER, S GLENNON, M. C REGAZZI, R DEENEY, J. T CORKEY, B. E |
| description | Several approaches were used to test the hypothesis proposing a role for acyl-CoA esters in nutrient-induced insulin release
(Prentki, M., and Matschinsky, F. M. (1987) Physiol. Rev. 67, 1185-1248; Corkey, B. E., Glennon, M. C., Chen, K. S., Deeney,
J. T., Matschinsky, F. M., and Prentki, M. (1989) J. Biol. Chem. 264, 21608-21612). Exogenous saturated long chain fatty acids
markedly potentiated glucose-induced insulin release and elevated long chain acyl-CoA esters in the clonal beta-cell line
(HIT). The secretory action depended on the fatty acid chain length, occurred in the range 3-20 microM (free concentration
of palmitate), and was reversible and inhibitable by the neuromodulator somatostatin. 2-Bromopalmitate, an inhibitor of carnitine
palmitoyl transferase I, suppressed the oxidation of endogenous fatty acids and promoted release of insulin. Only the nutrients
or the combination of nutrients that caused secretion elevated malonyl-CoA. The short-chain acyl-CoA profile of HIT cells
stimulated by various nutrients was determined in the presence of the nonstimulatory fuel glutamine. Glucose and leucine each
provoked similar changes in acyl-CoA compounds. Both secretagogues elevated malonyl-CoA 3-6-fold, whereas succinyl-CoA, free
CoASH, acetyl-CoA, and the free CoASH to acetyl-CoA ratio remained unaltered. Furthermore, only when inhibition of fatty acid
oxidation was associated with a rise in malonyl-CoA did the total (mitochondrial plus cytoplasmic) content of long chain acyl-CoA
esters correlate inversely with insulin release promoted by various nutrients. The results are consistent with the concept
that fuel stimuli cause a rise in malonyl-CoA which by inhibiting fatty acid oxidation increase cytosolic long chain acyl-CoA
esters. These data provide further support for a model in which malonyl-CoA and long chain acyl-CoAs esters serve as metabolic
coupling factors when pancreatic beta-cells are stimulated with glucose and other nutrient secretagogues. |
| doi_str_mv | 10.1016/s0021-9258(18)42624-5 |
| format | Article |
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(Prentki, M., and Matschinsky, F. M. (1987) Physiol. Rev. 67, 1185-1248; Corkey, B. E., Glennon, M. C., Chen, K. S., Deeney,
J. T., Matschinsky, F. M., and Prentki, M. (1989) J. Biol. Chem. 264, 21608-21612). Exogenous saturated long chain fatty acids
markedly potentiated glucose-induced insulin release and elevated long chain acyl-CoA esters in the clonal beta-cell line
(HIT). The secretory action depended on the fatty acid chain length, occurred in the range 3-20 microM (free concentration
of palmitate), and was reversible and inhibitable by the neuromodulator somatostatin. 2-Bromopalmitate, an inhibitor of carnitine
palmitoyl transferase I, suppressed the oxidation of endogenous fatty acids and promoted release of insulin. Only the nutrients
or the combination of nutrients that caused secretion elevated malonyl-CoA. The short-chain acyl-CoA profile of HIT cells
stimulated by various nutrients was determined in the presence of the nonstimulatory fuel glutamine. Glucose and leucine each
provoked similar changes in acyl-CoA compounds. Both secretagogues elevated malonyl-CoA 3-6-fold, whereas succinyl-CoA, free
CoASH, acetyl-CoA, and the free CoASH to acetyl-CoA ratio remained unaltered. Furthermore, only when inhibition of fatty acid
oxidation was associated with a rise in malonyl-CoA did the total (mitochondrial plus cytoplasmic) content of long chain acyl-CoA
esters correlate inversely with insulin release promoted by various nutrients. The results are consistent with the concept
that fuel stimuli cause a rise in malonyl-CoA which by inhibiting fatty acid oxidation increase cytosolic long chain acyl-CoA
esters. These data provide further support for a model in which malonyl-CoA and long chain acyl-CoAs esters serve as metabolic
coupling factors when pancreatic beta-cells are stimulated with glucose and other nutrient secretagogues.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1016/s0021-9258(18)42624-5</identifier><identifier>PMID: 1556096</identifier><identifier>CODEN: JBCHA3</identifier><language>eng</language><publisher>Bethesda, MD: American Society for Biochemistry and Molecular Biology</publisher><subject>Acyl Coenzyme A - metabolism ; acyl-CoA esters ; Animals ; Biological and medical sciences ; Cell Line ; Cell physiology ; Fatty Acids, Nonesterified - metabolism ; Fatty Acids, Nonesterified - pharmacology ; Fundamental and applied biological sciences. Psychology ; Glucose - pharmacology ; insulin ; Insulin - metabolism ; Insulin Secretion ; Islets of Langerhans ; Kinetics ; Malonyl Coenzyme A - metabolism ; Models, Biological ; Molecular and cellular biology ; Palmitates - pharmacology ; Palmitic Acid ; Palmitic Acids - metabolism ; Palmitic Acids - pharmacology ; Secretion. Exocytosis ; Serum Albumin, Bovine - pharmacology ; Structure-Activity Relationship</subject><ispartof>The Journal of biological chemistry, 1992-03, Vol.267 (9), p.5802-5810</ispartof><rights>1992 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-7e329feedf9cfa128ddba6380020136e7b16a8a9e5bd6e86d097d14dd998cc6a3</citedby><cites>FETCH-LOGICAL-c504t-7e329feedf9cfa128ddba6380020136e7b16a8a9e5bd6e86d097d14dd998cc6a3</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=5278145$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1556096$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>PRENTKI, M</creatorcontrib><creatorcontrib>VISCHER, S</creatorcontrib><creatorcontrib>GLENNON, M. C</creatorcontrib><creatorcontrib>REGAZZI, R</creatorcontrib><creatorcontrib>DEENEY, J. T</creatorcontrib><creatorcontrib>CORKEY, B. E</creatorcontrib><title>Malonyl-CoA and long chain acyl-CoA esters as metabolic coupling factors in nutrient-induced insulin secretion</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Several approaches were used to test the hypothesis proposing a role for acyl-CoA esters in nutrient-induced insulin release
(Prentki, M., and Matschinsky, F. M. (1987) Physiol. Rev. 67, 1185-1248; Corkey, B. E., Glennon, M. C., Chen, K. S., Deeney,
J. T., Matschinsky, F. M., and Prentki, M. (1989) J. Biol. Chem. 264, 21608-21612). Exogenous saturated long chain fatty acids
markedly potentiated glucose-induced insulin release and elevated long chain acyl-CoA esters in the clonal beta-cell line
(HIT). The secretory action depended on the fatty acid chain length, occurred in the range 3-20 microM (free concentration
of palmitate), and was reversible and inhibitable by the neuromodulator somatostatin. 2-Bromopalmitate, an inhibitor of carnitine
palmitoyl transferase I, suppressed the oxidation of endogenous fatty acids and promoted release of insulin. Only the nutrients
or the combination of nutrients that caused secretion elevated malonyl-CoA. The short-chain acyl-CoA profile of HIT cells
stimulated by various nutrients was determined in the presence of the nonstimulatory fuel glutamine. Glucose and leucine each
provoked similar changes in acyl-CoA compounds. Both secretagogues elevated malonyl-CoA 3-6-fold, whereas succinyl-CoA, free
CoASH, acetyl-CoA, and the free CoASH to acetyl-CoA ratio remained unaltered. Furthermore, only when inhibition of fatty acid
oxidation was associated with a rise in malonyl-CoA did the total (mitochondrial plus cytoplasmic) content of long chain acyl-CoA
esters correlate inversely with insulin release promoted by various nutrients. The results are consistent with the concept
that fuel stimuli cause a rise in malonyl-CoA which by inhibiting fatty acid oxidation increase cytosolic long chain acyl-CoA
esters. These data provide further support for a model in which malonyl-CoA and long chain acyl-CoAs esters serve as metabolic
coupling factors when pancreatic beta-cells are stimulated with glucose and other nutrient secretagogues.</description><subject>Acyl Coenzyme A - metabolism</subject><subject>acyl-CoA esters</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>Cell physiology</subject><subject>Fatty Acids, Nonesterified - metabolism</subject><subject>Fatty Acids, Nonesterified - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glucose - pharmacology</subject><subject>insulin</subject><subject>Insulin - metabolism</subject><subject>Insulin Secretion</subject><subject>Islets of Langerhans</subject><subject>Kinetics</subject><subject>Malonyl Coenzyme A - metabolism</subject><subject>Models, Biological</subject><subject>Molecular and cellular biology</subject><subject>Palmitates - pharmacology</subject><subject>Palmitic Acid</subject><subject>Palmitic Acids - metabolism</subject><subject>Palmitic Acids - pharmacology</subject><subject>Secretion. Exocytosis</subject><subject>Serum Albumin, Bovine - pharmacology</subject><subject>Structure-Activity Relationship</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU-LFDEQxYMo67j6ERYaEdFDayrdSSfHZfAfrHhQwVuoTqp3Ij3JmHQj--3NOMN6NJeQer9XSeoxdgX8DXBQbwvnAlojpH4F-nUvlOhb-YBtgOuu7ST8eMg298hj9qSUn7yu3sAFuwApFTdqw-JnnFO8m9ttum4w-qaebhu3wxAbdOc6lYVyabA0e1pwTHNwjUvrYQ6VndAtqarVENclB4pLG6JfHflaK2uFmkIu0xJSfMoeTTgXenbeL9n39---bT-2N18-fNpe37RO8n5pB-qEmYj8ZNyEILT3I6pO1_9w6BQNIyjUaEiOXpFWnpvBQ--9Mdo5hd0le3nqe8jp11rfb_ehOJpnjJTWYgehh15y9V8QFAwcQFRQnkCXUymZJnvIYY_5zgK3x0Ds1-O07XHaFrT9G4iV1Xd1vmAd9-T_uU4JVP3FWcficJ4yRhfKPSbFoKE_tnl-wnbhdvc7ZLJjSG5HeyvUYI2VmovuDxZ3oAY</recordid><startdate>19920325</startdate><enddate>19920325</enddate><creator>PRENTKI, M</creator><creator>VISCHER, S</creator><creator>GLENNON, M. 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E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-7e329feedf9cfa128ddba6380020136e7b16a8a9e5bd6e86d097d14dd998cc6a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Acyl Coenzyme A - metabolism</topic><topic>acyl-CoA esters</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Line</topic><topic>Cell physiology</topic><topic>Fatty Acids, Nonesterified - metabolism</topic><topic>Fatty Acids, Nonesterified - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glucose - pharmacology</topic><topic>insulin</topic><topic>Insulin - metabolism</topic><topic>Insulin Secretion</topic><topic>Islets of Langerhans</topic><topic>Kinetics</topic><topic>Malonyl Coenzyme A - metabolism</topic><topic>Models, Biological</topic><topic>Molecular and cellular biology</topic><topic>Palmitates - pharmacology</topic><topic>Palmitic Acid</topic><topic>Palmitic Acids - metabolism</topic><topic>Palmitic Acids - pharmacology</topic><topic>Secretion. Exocytosis</topic><topic>Serum Albumin, Bovine - pharmacology</topic><topic>Structure-Activity Relationship</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>PRENTKI, M</creatorcontrib><creatorcontrib>VISCHER, S</creatorcontrib><creatorcontrib>GLENNON, M. C</creatorcontrib><creatorcontrib>REGAZZI, R</creatorcontrib><creatorcontrib>DEENEY, J. T</creatorcontrib><creatorcontrib>CORKEY, B. 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E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Malonyl-CoA and long chain acyl-CoA esters as metabolic coupling factors in nutrient-induced insulin secretion</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>1992-03-25</date><risdate>1992</risdate><volume>267</volume><issue>9</issue><spage>5802</spage><epage>5810</epage><pages>5802-5810</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><coden>JBCHA3</coden><abstract>Several approaches were used to test the hypothesis proposing a role for acyl-CoA esters in nutrient-induced insulin release
(Prentki, M., and Matschinsky, F. M. (1987) Physiol. Rev. 67, 1185-1248; Corkey, B. E., Glennon, M. C., Chen, K. S., Deeney,
J. T., Matschinsky, F. M., and Prentki, M. (1989) J. Biol. Chem. 264, 21608-21612). Exogenous saturated long chain fatty acids
markedly potentiated glucose-induced insulin release and elevated long chain acyl-CoA esters in the clonal beta-cell line
(HIT). The secretory action depended on the fatty acid chain length, occurred in the range 3-20 microM (free concentration
of palmitate), and was reversible and inhibitable by the neuromodulator somatostatin. 2-Bromopalmitate, an inhibitor of carnitine
palmitoyl transferase I, suppressed the oxidation of endogenous fatty acids and promoted release of insulin. Only the nutrients
or the combination of nutrients that caused secretion elevated malonyl-CoA. The short-chain acyl-CoA profile of HIT cells
stimulated by various nutrients was determined in the presence of the nonstimulatory fuel glutamine. Glucose and leucine each
provoked similar changes in acyl-CoA compounds. Both secretagogues elevated malonyl-CoA 3-6-fold, whereas succinyl-CoA, free
CoASH, acetyl-CoA, and the free CoASH to acetyl-CoA ratio remained unaltered. Furthermore, only when inhibition of fatty acid
oxidation was associated with a rise in malonyl-CoA did the total (mitochondrial plus cytoplasmic) content of long chain acyl-CoA
esters correlate inversely with insulin release promoted by various nutrients. The results are consistent with the concept
that fuel stimuli cause a rise in malonyl-CoA which by inhibiting fatty acid oxidation increase cytosolic long chain acyl-CoA
esters. These data provide further support for a model in which malonyl-CoA and long chain acyl-CoAs esters serve as metabolic
coupling factors when pancreatic beta-cells are stimulated with glucose and other nutrient secretagogues.</abstract><cop>Bethesda, MD</cop><pub>American Society for Biochemistry and Molecular Biology</pub><pmid>1556096</pmid><doi>10.1016/s0021-9258(18)42624-5</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | The Journal of biological chemistry, 1992-03, Vol.267 (9), p.5802-5810 |
| issn | 0021-9258 1083-351X |
| language | eng |
| recordid | cdi_proquest_miscellaneous_72874506 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Acyl Coenzyme A - metabolism acyl-CoA esters Animals Biological and medical sciences Cell Line Cell physiology Fatty Acids, Nonesterified - metabolism Fatty Acids, Nonesterified - pharmacology Fundamental and applied biological sciences. Psychology Glucose - pharmacology insulin Insulin - metabolism Insulin Secretion Islets of Langerhans Kinetics Malonyl Coenzyme A - metabolism Models, Biological Molecular and cellular biology Palmitates - pharmacology Palmitic Acid Palmitic Acids - metabolism Palmitic Acids - pharmacology Secretion. Exocytosis Serum Albumin, Bovine - pharmacology Structure-Activity Relationship |
| title | Malonyl-CoA and long chain acyl-CoA esters as metabolic coupling factors in nutrient-induced insulin secretion |
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