Olanzapine treatment is associated with reduced high molecular weight adiponectin in serum: a potential mechanism for olanzapine-induced insulin resistance in patients with schizophrenia.
Identifieur interne : 002256 ( PubMed/Corpus ); précédent : 002255; suivant : 002257Olanzapine treatment is associated with reduced high molecular weight adiponectin in serum: a potential mechanism for olanzapine-induced insulin resistance in patients with schizophrenia.
Auteurs : Ayanthi A. Richards ; Ingrid J. Hickman ; Amy Y-H Wang ; Amanda L. Jones ; Felicity Newell ; Bryan J. Mowry ; Jonathan P. Whitehead ; Johannes B. Prins ; Graeme A. MacdonaldSource :
- Journal of clinical psychopharmacology [ 0271-0749 ] ; 2006.
English descriptors
- KwdEn :
- Adipocytes (drug effects), Adipocytes (metabolism), Adiponectin (blood), Adiponectin (chemistry), Adult, Antipsychotic Agents (adverse effects), Antipsychotic Agents (therapeutic use), Benzodiazepines (adverse effects), Benzodiazepines (therapeutic use), Blood Glucose (metabolism), Cells, Cultured, Female, Humans, Insulin Resistance, Male, Molecular Weight, Olanzapine, Schizophrenia (complications), Schizophrenia (drug therapy).
- MESH :
- chemical , adverse effects : Antipsychotic Agents, Benzodiazepines.
- chemical , blood : Adiponectin.
- chemical , chemistry : Adiponectin.
- complications : Schizophrenia.
- drug effects : Adipocytes.
- drug therapy : Schizophrenia.
- metabolism : Adipocytes, Blood Glucose.
- chemical , therapeutic use : Antipsychotic Agents, Benzodiazepines.
- Adult, Cells, Cultured, Female, Humans, Insulin Resistance, Male, Molecular Weight, Olanzapine.
Abstract
Treatment of schizophrenia with olanzapine and other atypical antipsychotic agents is associated with insulin resistance and diabetes mellitus. The mechanism for this is not understood. Adiponectin is an insulin-sensitizing cytokine secreted by adipocytes. It is present in serum in multimers of varying size. Trimers and hexamers are referred to as low molecular weight (LMW) adiponectin. Larger multimers (12-, 18-, and 24-mers) have been designated high molecular weight (HMW) adiponectin and seem responsible for the insulin-sensitizing action of this adipokine. The aim of this study was to examine total adiponectin and LMW and HMW multimers in serum from patients with schizophrenia treated with either olanzapine (n = 9) or other typical antipsychotics (n = 9) and compare results with 16 healthy sex-, body mass index-, and age-matched controls. The effects of olanzapine on adiponectin protein expression and secretion in in vitro-differentiated primary human adipocytes were also examined. Patients receiving olanzapine had significantly lower total serum adiponectin as compared with those on conventional treatment and controls (5.23 +/- 1.53 ng/mL vs. 8.20 +/- 3.77 ng/mL and 8.78 +/- 3.8 ng/mL; P < 0.05 and P < 0.01, respectively). The HMW adiponectin was also reduced in patients on olanzapine as compared with the disease and healthy control groups (1.67 +/- 0.96 ng/mL vs. 3.87 +/- 2.69 ng/mL and 4.07 +/- 3.2 ng/mL; P < 0.05 for both). The LMW adiponectin was not different between patient groups (P = 0.15) but lower in patients on olanzapine as compared with controls (3.56 +/- 0.85 ng/mL vs. 4.70 +/- 1.4 ng/mL; P < 0.05). In vitro, short duration (up to 7 days) olanzapine exposure had no effect on total adiponectin expression or multimer composition of secreted protein. In summary, this study demonstrates a correlation between olanzapine treatment and reduced serum adiponectin, particularly HMW multimers. This may not be a direct effect of olanzapine on adipocyte expression or secretion of adiponectin. These observations provide insights into possible mechanisms for the association between olanzapine treatment and insulin resistance.
DOI: 10.1097/01.jcp.0000218404.64619.52
PubMed: 16702887
Links to Exploration step
pubmed:16702887Le document en format XML
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Jones</name></author><author><name sortKey="Newell, Felicity" sort="Newell, Felicity" uniqKey="Newell F" first="Felicity" last="Newell">Felicity Newell</name></author><author><name sortKey="Mowry, Bryan J" sort="Mowry, Bryan J" uniqKey="Mowry B" first="Bryan J" last="Mowry">Bryan J. Mowry</name></author><author><name sortKey="Whitehead, Jonathan P" sort="Whitehead, Jonathan P" uniqKey="Whitehead J" first="Jonathan P" last="Whitehead">Jonathan P. Whitehead</name></author><author><name sortKey="Prins, Johannes B" sort="Prins, Johannes B" uniqKey="Prins J" first="Johannes B" last="Prins">Johannes B. Prins</name></author><author><name sortKey="Macdonald, Graeme A" sort="Macdonald, Graeme A" uniqKey="Macdonald G" first="Graeme A" last="Macdonald">Graeme A. 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Richards</name><affiliation><nlm:affiliation>Centre for Diabetes and Endocrine Research, The University of Queensland, Brisbane, Queensland, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Hickman, Ingrid J" sort="Hickman, Ingrid J" uniqKey="Hickman I" first="Ingrid J" last="Hickman">Ingrid J. Hickman</name></author><author><name sortKey="Wang, Amy Y H" sort="Wang, Amy Y H" uniqKey="Wang A" first="Amy Y-H" last="Wang">Amy Y-H Wang</name></author><author><name sortKey="Jones, Amanda L" sort="Jones, Amanda L" uniqKey="Jones A" first="Amanda L" last="Jones">Amanda L. Jones</name></author><author><name sortKey="Newell, Felicity" sort="Newell, Felicity" uniqKey="Newell F" first="Felicity" last="Newell">Felicity Newell</name></author><author><name sortKey="Mowry, Bryan J" sort="Mowry, Bryan J" uniqKey="Mowry B" first="Bryan J" last="Mowry">Bryan J. Mowry</name></author><author><name sortKey="Whitehead, Jonathan P" sort="Whitehead, Jonathan P" uniqKey="Whitehead J" first="Jonathan P" last="Whitehead">Jonathan P. Whitehead</name></author><author><name sortKey="Prins, Johannes B" sort="Prins, Johannes B" uniqKey="Prins J" first="Johannes B" last="Prins">Johannes B. Prins</name></author><author><name sortKey="Macdonald, Graeme A" sort="Macdonald, Graeme A" uniqKey="Macdonald G" first="Graeme A" last="Macdonald">Graeme A. Macdonald</name></author></analytic><series><title level="j">Journal of clinical psychopharmacology</title><idno type="ISSN">0271-0749</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adipocytes (drug effects)</term><term>Adipocytes (metabolism)</term><term>Adiponectin (blood)</term><term>Adiponectin (chemistry)</term><term>Adult</term><term>Antipsychotic Agents (adverse effects)</term><term>Antipsychotic Agents (therapeutic use)</term><term>Benzodiazepines (adverse effects)</term><term>Benzodiazepines (therapeutic use)</term><term>Blood Glucose (metabolism)</term><term>Cells, Cultured</term><term>Female</term><term>Humans</term><term>Insulin Resistance</term><term>Male</term><term>Molecular Weight</term><term>Olanzapine</term><term>Schizophrenia (complications)</term><term>Schizophrenia (drug therapy)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antipsychotic Agents</term><term>Benzodiazepines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Adiponectin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Adiponectin</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Schizophrenia</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Adipocytes</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Schizophrenia</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Adipocytes</term><term>Blood Glucose</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antipsychotic Agents</term><term>Benzodiazepines</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Cells, Cultured</term><term>Female</term><term>Humans</term><term>Insulin Resistance</term><term>Male</term><term>Molecular Weight</term><term>Olanzapine</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Treatment of schizophrenia with olanzapine and other atypical antipsychotic agents is associated with insulin resistance and diabetes mellitus. The mechanism for this is not understood. Adiponectin is an insulin-sensitizing cytokine secreted by adipocytes. It is present in serum in multimers of varying size. Trimers and hexamers are referred to as low molecular weight (LMW) adiponectin. Larger multimers (12-, 18-, and 24-mers) have been designated high molecular weight (HMW) adiponectin and seem responsible for the insulin-sensitizing action of this adipokine. The aim of this study was to examine total adiponectin and LMW and HMW multimers in serum from patients with schizophrenia treated with either olanzapine (n = 9) or other typical antipsychotics (n = 9) and compare results with 16 healthy sex-, body mass index-, and age-matched controls. The effects of olanzapine on adiponectin protein expression and secretion in in vitro-differentiated primary human adipocytes were also examined. Patients receiving olanzapine had significantly lower total serum adiponectin as compared with those on conventional treatment and controls (5.23 +/- 1.53 ng/mL vs. 8.20 +/- 3.77 ng/mL and 8.78 +/- 3.8 ng/mL; P < 0.05 and P < 0.01, respectively). The HMW adiponectin was also reduced in patients on olanzapine as compared with the disease and healthy control groups (1.67 +/- 0.96 ng/mL vs. 3.87 +/- 2.69 ng/mL and 4.07 +/- 3.2 ng/mL; P < 0.05 for both). The LMW adiponectin was not different between patient groups (P = 0.15) but lower in patients on olanzapine as compared with controls (3.56 +/- 0.85 ng/mL vs. 4.70 +/- 1.4 ng/mL; P < 0.05). In vitro, short duration (up to 7 days) olanzapine exposure had no effect on total adiponectin expression or multimer composition of secreted protein. In summary, this study demonstrates a correlation between olanzapine treatment and reduced serum adiponectin, particularly HMW multimers. This may not be a direct effect of olanzapine on adipocyte expression or secretion of adiponectin. These observations provide insights into possible mechanisms for the association between olanzapine treatment and insulin resistance.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16702887</PMID><DateCompleted><Year>2006</Year><Month>08</Month><Day>10</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>01</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0271-0749</ISSN><JournalIssue CitedMedium="Print"><Volume>26</Volume><Issue>3</Issue><PubDate><Year>2006</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Journal of clinical psychopharmacology</Title><ISOAbbreviation>J Clin Psychopharmacol</ISOAbbreviation></Journal><ArticleTitle>Olanzapine treatment is associated with reduced high molecular weight adiponectin in serum: a potential mechanism for olanzapine-induced insulin resistance in patients with schizophrenia.</ArticleTitle><Pagination><MedlinePgn>232-7</MedlinePgn></Pagination><Abstract><AbstractText>Treatment of schizophrenia with olanzapine and other atypical antipsychotic agents is associated with insulin resistance and diabetes mellitus. The mechanism for this is not understood. Adiponectin is an insulin-sensitizing cytokine secreted by adipocytes. It is present in serum in multimers of varying size. Trimers and hexamers are referred to as low molecular weight (LMW) adiponectin. Larger multimers (12-, 18-, and 24-mers) have been designated high molecular weight (HMW) adiponectin and seem responsible for the insulin-sensitizing action of this adipokine. The aim of this study was to examine total adiponectin and LMW and HMW multimers in serum from patients with schizophrenia treated with either olanzapine (n = 9) or other typical antipsychotics (n = 9) and compare results with 16 healthy sex-, body mass index-, and age-matched controls. The effects of olanzapine on adiponectin protein expression and secretion in in vitro-differentiated primary human adipocytes were also examined. Patients receiving olanzapine had significantly lower total serum adiponectin as compared with those on conventional treatment and controls (5.23 +/- 1.53 ng/mL vs. 8.20 +/- 3.77 ng/mL and 8.78 +/- 3.8 ng/mL; P < 0.05 and P < 0.01, respectively). The HMW adiponectin was also reduced in patients on olanzapine as compared with the disease and healthy control groups (1.67 +/- 0.96 ng/mL vs. 3.87 +/- 2.69 ng/mL and 4.07 +/- 3.2 ng/mL; P < 0.05 for both). The LMW adiponectin was not different between patient groups (P = 0.15) but lower in patients on olanzapine as compared with controls (3.56 +/- 0.85 ng/mL vs. 4.70 +/- 1.4 ng/mL; P < 0.05). In vitro, short duration (up to 7 days) olanzapine exposure had no effect on total adiponectin expression or multimer composition of secreted protein. In summary, this study demonstrates a correlation between olanzapine treatment and reduced serum adiponectin, particularly HMW multimers. This may not be a direct effect of olanzapine on adipocyte expression or secretion of adiponectin. These observations provide insights into possible mechanisms for the association between olanzapine treatment and insulin resistance.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Richards</LastName><ForeName>Ayanthi A</ForeName><Initials>AA</Initials><AffiliationInfo><Affiliation>Centre for Diabetes and Endocrine Research, The University of Queensland, Brisbane, Queensland, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hickman</LastName><ForeName>Ingrid J</ForeName><Initials>IJ</Initials></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Amy Y-H</ForeName><Initials>AY</Initials></Author><Author ValidYN="Y"><LastName>Jones</LastName><ForeName>Amanda L</ForeName><Initials>AL</Initials></Author><Author ValidYN="Y"><LastName>Newell</LastName><ForeName>Felicity</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Mowry</LastName><ForeName>Bryan J</ForeName><Initials>BJ</Initials></Author><Author ValidYN="Y"><LastName>Whitehead</LastName><ForeName>Jonathan P</ForeName><Initials>JP</Initials></Author><Author ValidYN="Y"><LastName>Prins</LastName><ForeName>Johannes B</ForeName><Initials>JB</Initials></Author><Author ValidYN="Y"><LastName>Macdonald</LastName><ForeName>Graeme A</ForeName><Initials>GA</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 MH59565</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 MH59566</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 MH59571</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 MH59586</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 MH59587</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 MH59588</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 MH60870</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 MH60879</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 MH61675</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Clin Psychopharmacol</MedlineTA><NlmUniqueID>8109496</NlmUniqueID><ISSNLinking>0271-0749</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D052242">Adiponectin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014150">Antipsychotic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>12794-10-4</RegistryNumber><NameOfSubstance UI="D001569">Benzodiazepines</NameOfSubstance></Chemical><Chemical><RegistryNumber>N7U69T4SZR</RegistryNumber><NameOfSubstance UI="D000077152">Olanzapine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017667" MajorTopicYN="N">Adipocytes</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" 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Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="Y">Insulin Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008970" MajorTopicYN="N">Molecular Weight</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000077152" MajorTopicYN="N">Olanzapine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012559" MajorTopicYN="N">Schizophrenia</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>5</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>8</Month><Day>11</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>5</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16702887</ArticleId><ArticleId IdType="doi">10.1097/01.jcp.0000218404.64619.52</ArticleId><ArticleId IdType="pii">00004714-200606000-00003</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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