Insulin receptors and insulin action in the brain: review and clinical implications
Identifieur interne : 002791 ( Main/Corpus ); précédent : 002790; suivant : 002792Insulin receptors and insulin action in the brain: review and clinical implications
Auteurs : R. J Schulingkamp ; T. C Pagano ; D. Hung ; R. B RaffaSource :
- Neuroscience and Biobehavioral Reviews [ 0149-7634 ] ; 2000.
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Abstract
Insulin receptors are known to be located on nerve cells in mammalian brain. The binding of insulin to dimerized receptors stimulates specialized transporter proteins that mediate the facilitated influx of glucose. However, neurons possess other mechanisms by which they obtain glucose, including transporters that are not insulin-dependent. Further, insulin receptors are unevenly distributed throughout the brain (with particularly high density in choroid plexus, olfactory bulb and regions of the striatum and cerebral cortex). Such factors imply that insulin, and insulin receptors, might have functions within the central nervous system in addition to those related to the supply of glucose. Indeed, invertebrate insulin-related peptides are synthesized in brain and serve as neurotransmitters or neuromodulators. The present review summarizes the structure, distribution and function of mammalian brain insulin receptors and the possible implications for central nervous system disorders. It is proposed that this is an under-studied subject of investigation.
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DOI: 10.1016/S0149-7634(00)00040-3
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Hung</name><affiliation><mods:affiliation>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</mods:affiliation></affiliation></author><author><name sortKey="Raffa, R B" sort="Raffa, R B" uniqKey="Raffa R" first="R. B" last="Raffa">R. 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J" last="Schulingkamp">R. J Schulingkamp</name><affiliation><mods:affiliation>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</mods:affiliation></affiliation></author><author><name sortKey="Pagano, T C" sort="Pagano, T C" uniqKey="Pagano T" first="T. C" last="Pagano">T. C Pagano</name><affiliation><mods:affiliation>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</mods:affiliation></affiliation></author><author><name sortKey="Hung, D" sort="Hung, D" uniqKey="Hung D" first="D" last="Hung">D. Hung</name><affiliation><mods:affiliation>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</mods:affiliation></affiliation></author><author><name sortKey="Raffa, R B" sort="Raffa, R B" uniqKey="Raffa R" first="R. B" last="Raffa">R. B Raffa</name><affiliation><mods:affiliation>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: rraffa@nimbus.temple.edu</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Neuroscience and Biobehavioral Reviews</title><title level="j" type="abbrev">NBR</title><idno type="ISSN">0149-7634</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000">2000</date><biblScope unit="volume">24</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="855">855</biblScope><biblScope unit="page" to="872">872</biblScope></imprint><idno type="ISSN">0149-7634</idno></series><idno type="istex">F97C6A09CE79475ECB22403F47D79E8E4D9AF526</idno><idno type="DOI">10.1016/S0149-7634(00)00040-3</idno><idno type="PII">S0149-7634(00)00040-3</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0149-7634</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Brain</term><term>CNS disorders</term><term>Glucose transporter</term><term>Insulin receptor</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Insulin receptors are known to be located on nerve cells in mammalian brain. The binding of insulin to dimerized receptors stimulates specialized transporter proteins that mediate the facilitated influx of glucose. However, neurons possess other mechanisms by which they obtain glucose, including transporters that are not insulin-dependent. Further, insulin receptors are unevenly distributed throughout the brain (with particularly high density in choroid plexus, olfactory bulb and regions of the striatum and cerebral cortex). Such factors imply that insulin, and insulin receptors, might have functions within the central nervous system in addition to those related to the supply of glucose. Indeed, invertebrate insulin-related peptides are synthesized in brain and serve as neurotransmitters or neuromodulators. The present review summarizes the structure, distribution and function of mammalian brain insulin receptors and the possible implications for central nervous system disorders. It is proposed that this is an under-studied subject of investigation.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>R.J Schulingkamp</name><affiliations><json:string>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</json:string></affiliations></json:item><json:item><name>T.C Pagano</name><affiliations><json:string>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</json:string></affiliations></json:item><json:item><name>D Hung</name><affiliations><json:string>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</json:string></affiliations></json:item><json:item><name>R.B Raffa</name><affiliations><json:string>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</json:string><json:string>E-mail: rraffa@nimbus.temple.edu</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Insulin receptor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Brain</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Glucose transporter</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CNS disorders</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Insulin receptors are known to be located on nerve cells in mammalian brain. The binding of insulin to dimerized receptors stimulates specialized transporter proteins that mediate the facilitated influx of glucose. However, neurons possess other mechanisms by which they obtain glucose, including transporters that are not insulin-dependent. Further, insulin receptors are unevenly distributed throughout the brain (with particularly high density in choroid plexus, olfactory bulb and regions of the striatum and cerebral cortex). Such factors imply that insulin, and insulin receptors, might have functions within the central nervous system in addition to those related to the supply of glucose. Indeed, invertebrate insulin-related peptides are synthesized in brain and serve as neurotransmitters or neuromodulators. The present review summarizes the structure, distribution and function of mammalian brain insulin receptors and the possible implications for central nervous system disorders. 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Highest densities are indicated by lighter shades. From Werther et al.[1] with permission, © The Endocrine Society. Abbreviations: ac, anterior commisure; cc, corpus callosum; f, fornix; ic, internal capsule; mpo, medial preoptic area; on, optic nerve; ot, optic tract; py, pyramidal tract; rh, nucleus rhomboidus; rspl, retrosplenial cortex; pv, paraventricular nucleus of thalamus; vdb, vertical limb of diagonal band of Broca; wm, white matter of cerebellum.</note><note type="content">Fig. 2: The insulin receptor (InsR) and glucose internalization. The inherent tyrosine-kinase activity of the β subunit of the InsR, normally inhibited by the α subunit, is disinhibited by the binding of insulin molecule(s) to the α subunit(s) of the InsR. Greater insulin affinity is associated with dimerized InsR. Activation of InsR can result in translocation of glucose transporter molecules (here represented by GLUT- 4) to the membrane surface and mediation of glusose entry into the cell. –S–S–=disulfide bridges.</note><note type="content">Fig. 3: The interrelationship between brain insulin receptors (InsRb) and neurotransmitter function. InsRb located on astrocytes modulate the entry of glucose to maintain the homeostatic control levels associated with β-adrenoceptor (β-AR) activity. InsRb located on neuronal cell bodies inhibit the expression of neuropeptide Y (NPY) levels and, hence, attenuate the modulatory role of NPY on norepinephrine (NE) neurotransmitter function. InsRb might also be located presynaptically. In addition, insulin inhibits the neuronal reuptake of NE and stimulates the neuronal reuptake of 5-HT (serotonin) (not shown).</note><note type="content">Table 1: Localization of insulin receptors in rat brain identified using 125I-labeled insulin and computer-assisted densitometry [2,3]</note><note type="content">Table 2: Relative insulin and insulin receptor content in rat brain, arranged from highest to lowest [16,19]</note><note type="content">Table 3: Passage of insulin across the blood–brain-barrier [98]</note><note type="content">Table 4: Representative studies related to glucose and depression</note><note type="content">Table 5: Representative studies related to glucose and Huntington disease</note><note type="content">Table 6: Representative studies related to InsRb and Parkinson disease</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Insulin receptors and insulin action in the brain: review and clinical implications</title><author><persName><forename type="first">R.J</forename><surname>Schulingkamp</surname></persName><affiliation>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</affiliation></author><author><persName><forename type="first">T.C</forename><surname>Pagano</surname></persName><affiliation>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</affiliation></author><author><persName><forename type="first">D</forename><surname>Hung</surname></persName><affiliation>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</affiliation></author><author><persName><forename type="first">R.B</forename><surname>Raffa</surname></persName><email>rraffa@nimbus.temple.edu</email><note type="correspondence"><p>Corresponding author. Tel.: +1-215-707-4976; fax: +1-215-707-5228</p></note><affiliation>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</affiliation></author></analytic><monogr><title level="j">Neuroscience and Biobehavioral Reviews</title><title level="j" type="abbrev">NBR</title><idno type="pISSN">0149-7634</idno><idno type="PII">S0149-7634(00)X0035-8</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000"></date><biblScope unit="volume">24</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="855">855</biblScope><biblScope unit="page" to="872">872</biblScope></imprint></monogr><idno type="istex">F97C6A09CE79475ECB22403F47D79E8E4D9AF526</idno><idno type="DOI">10.1016/S0149-7634(00)00040-3</idno><idno type="PII">S0149-7634(00)00040-3</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2000</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Insulin receptors are known to be located on nerve cells in mammalian brain. The binding of insulin to dimerized receptors stimulates specialized transporter proteins that mediate the facilitated influx of glucose. However, neurons possess other mechanisms by which they obtain glucose, including transporters that are not insulin-dependent. Further, insulin receptors are unevenly distributed throughout the brain (with particularly high density in choroid plexus, olfactory bulb and regions of the striatum and cerebral cortex). Such factors imply that insulin, and insulin receptors, might have functions within the central nervous system in addition to those related to the supply of glucose. Indeed, invertebrate insulin-related peptides are synthesized in brain and serve as neurotransmitters or neuromodulators. The present review summarizes the structure, distribution and function of mammalian brain insulin receptors and the possible implications for central nervous system disorders. It is proposed that this is an under-studied subject of investigation.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Insulin receptor</term></item><item><term>Brain</term></item><item><term>Glucose transporter</term></item><item><term>CNS disorders</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2000-08-22">Registration</change><change when="2000-08-15">Modified</change><change when="2000">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: ce:floats; body; tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"><istex:entity SYSTEM="gr1" NDATA="IMAGE" name="gr1"></istex:entity><istex:entity SYSTEM="gr2" NDATA="IMAGE" name="gr2"></istex:entity><istex:entity SYSTEM="gr3" NDATA="IMAGE" name="gr3"></istex:entity></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>NBR</jid><aid>460</aid><ce:pii>S0149-7634(00)00040-3</ce:pii><ce:doi>10.1016/S0149-7634(00)00040-3</ce:doi><ce:copyright type="full-transfer" year="2000">Elsevier Science Ltd</ce:copyright></item-info><head><ce:title>Insulin receptors and insulin action in the brain: review and clinical implications</ce:title><ce:author-group><ce:author><ce:given-name>R.J</ce:given-name><ce:surname>Schulingkamp</ce:surname></ce:author><ce:author><ce:given-name>T.C</ce:given-name><ce:surname>Pagano</ce:surname></ce:author><ce:author><ce:given-name>D</ce:given-name><ce:surname>Hung</ce:surname></ce:author><ce:author><ce:given-name>R.B</ce:given-name><ce:surname>Raffa</ce:surname><ce:cross-ref refid="CORR1">*</ce:cross-ref><ce:e-address>rraffa@nimbus.temple.edu</ce:e-address></ce:author><ce:affiliation><ce:textfn>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</ce:textfn></ce:affiliation><ce:correspondence id="CORR1"><ce:label>*</ce:label><ce:text>Corresponding author. Tel.: +1-215-707-4976; fax: +1-215-707-5228</ce:text></ce:correspondence></ce:author-group><ce:date-received day="18" month="5" year="2000"></ce:date-received><ce:date-revised day="15" month="8" year="2000"></ce:date-revised><ce:date-accepted day="22" month="8" year="2000"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Insulin receptors are known to be located on nerve cells in mammalian brain. The binding of insulin to dimerized receptors stimulates specialized transporter proteins that mediate the facilitated influx of glucose. However, neurons possess other mechanisms by which they obtain glucose, including transporters that are not insulin-dependent. Further, insulin receptors are unevenly distributed throughout the brain (with particularly high density in choroid plexus, olfactory bulb and regions of the striatum and cerebral cortex). Such factors imply that insulin, and insulin receptors, might have functions within the central nervous system in addition to those related to the supply of glucose. Indeed, invertebrate insulin-related peptides are synthesized in brain and serve as neurotransmitters or neuromodulators. The present review summarizes the structure, distribution and function of mammalian brain insulin receptors and the possible implications for central nervous system disorders. It is proposed that this is an under-studied subject of investigation.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword" xml:lang="en"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Insulin receptor</ce:text></ce:keyword><ce:keyword><ce:text>Brain</ce:text></ce:keyword><ce:keyword><ce:text>Glucose transporter</ce:text></ce:keyword><ce:keyword><ce:text>CNS disorders</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Insulin receptors and insulin action in the brain: review and clinical implications</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Insulin receptors and insulin action in the brain: review and clinical implications</title></titleInfo><name type="personal"><namePart type="given">R.J</namePart><namePart type="family">Schulingkamp</namePart><affiliation>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T.C</namePart><namePart type="family">Pagano</namePart><affiliation>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Hung</namePart><affiliation>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.B</namePart><namePart type="family">Raffa</namePart><affiliation>Department of Pharmaceutical Sciences, Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, USA</affiliation><affiliation>E-mail: rraffa@nimbus.temple.edu</affiliation><description>Corresponding author. Tel.: +1-215-707-4976; fax: +1-215-707-5228</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2000</dateIssued><dateValid encoding="w3cdtf">2000-08-22</dateValid><dateModified encoding="w3cdtf">2000-08-15</dateModified><copyrightDate encoding="w3cdtf">2000</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Insulin receptors are known to be located on nerve cells in mammalian brain. The binding of insulin to dimerized receptors stimulates specialized transporter proteins that mediate the facilitated influx of glucose. However, neurons possess other mechanisms by which they obtain glucose, including transporters that are not insulin-dependent. Further, insulin receptors are unevenly distributed throughout the brain (with particularly high density in choroid plexus, olfactory bulb and regions of the striatum and cerebral cortex). Such factors imply that insulin, and insulin receptors, might have functions within the central nervous system in addition to those related to the supply of glucose. Indeed, invertebrate insulin-related peptides are synthesized in brain and serve as neurotransmitters or neuromodulators. The present review summarizes the structure, distribution and function of mammalian brain insulin receptors and the possible implications for central nervous system disorders. It is proposed that this is an under-studied subject of investigation.</abstract><note type="content">Fig. 1: Autoradiographs of 125I-insulin binding to coronal (a)–(h) and sagittal (i) sections of rat brain. Highest densities are indicated by lighter shades. From Werther et al.[1] with permission, © The Endocrine Society. Abbreviations: ac, anterior commisure; cc, corpus callosum; f, fornix; ic, internal capsule; mpo, medial preoptic area; on, optic nerve; ot, optic tract; py, pyramidal tract; rh, nucleus rhomboidus; rspl, retrosplenial cortex; pv, paraventricular nucleus of thalamus; vdb, vertical limb of diagonal band of Broca; wm, white matter of cerebellum.</note><note type="content">Fig. 2: The insulin receptor (InsR) and glucose internalization. The inherent tyrosine-kinase activity of the β subunit of the InsR, normally inhibited by the α subunit, is disinhibited by the binding of insulin molecule(s) to the α subunit(s) of the InsR. Greater insulin affinity is associated with dimerized InsR. Activation of InsR can result in translocation of glucose transporter molecules (here represented by GLUT- 4) to the membrane surface and mediation of glusose entry into the cell. –S–S–=disulfide bridges.</note><note type="content">Fig. 3: The interrelationship between brain insulin receptors (InsRb) and neurotransmitter function. InsRb located on astrocytes modulate the entry of glucose to maintain the homeostatic control levels associated with β-adrenoceptor (β-AR) activity. InsRb located on neuronal cell bodies inhibit the expression of neuropeptide Y (NPY) levels and, hence, attenuate the modulatory role of NPY on norepinephrine (NE) neurotransmitter function. InsRb might also be located presynaptically. In addition, insulin inhibits the neuronal reuptake of NE and stimulates the neuronal reuptake of 5-HT (serotonin) (not shown).</note><note type="content">Table 1: Localization of insulin receptors in rat brain identified using 125I-labeled insulin and computer-assisted densitometry [2,3]</note><note type="content">Table 2: Relative insulin and insulin receptor content in rat brain, arranged from highest to lowest [16,19]</note><note type="content">Table 3: Passage of insulin across the blood–brain-barrier [98]</note><note type="content">Table 4: Representative studies related to glucose and depression</note><note type="content">Table 5: Representative studies related to glucose and Huntington disease</note><note type="content">Table 6: Representative studies related to InsRb and Parkinson disease</note><subject lang="en"><genre>Keywords</genre><topic>Insulin receptor</topic><topic>Brain</topic><topic>Glucose transporter</topic><topic>CNS disorders</topic></subject><relatedItem type="host"><titleInfo><title>Neuroscience and Biobehavioral Reviews</title></titleInfo><titleInfo type="abbreviated"><title>NBR</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">200012</dateIssued></originInfo><identifier type="ISSN">0149-7634</identifier><identifier type="PII">S0149-7634(00)X0035-8</identifier><part><date>200012</date><detail type="volume"><number>24</number><caption>vol.</caption></detail><detail type="issue"><number>8</number><caption>no.</caption></detail><extent unit="issue pages"><start>777</start><end>872</end></extent><extent unit="pages"><start>855</start><end>872</end></extent></part></relatedItem><identifier type="istex">F97C6A09CE79475ECB22403F47D79E8E4D9AF526</identifier><identifier type="DOI">10.1016/S0149-7634(00)00040-3</identifier><identifier type="PII">S0149-7634(00)00040-3</identifier><accessCondition type="use and reproduction" contentType="">© 2000Elsevier Science Ltd</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>Elsevier Science Ltd, ©2000</recordOrigin></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/F97C6A09CE79475ECB22403F47D79E8E4D9AF526/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</classCode><classCode scheme="WOS">BEHAVIORAL SCIENCES</classCode><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments></istex></record>Pour manipuler ce document sous Unix (Dilib)
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