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Article: Testosterone selectively reduces the high molecular weight form of adiponectin by inhibiting its secretion from adipocytes

TitleTestosterone selectively reduces the high molecular weight form of adiponectin by inhibiting its secretion from adipocytes
Authors
Issue Date2005
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
Citation
Journal Of Biological Chemistry, 2005, v. 280 n. 18, p. 18073-18080 How to Cite?
AbstractThe antidiabetic hormone adiponectin circulates in blood as several oligomeric complexes, and the ratios between them are critical in determining insulin sensitivity. In this study we investigated the role of testosterone in regulating the oligomeric complex distribution of adiponectin. Gel filtration analysis revealed that circulating adiponectin existed as the forms of high molecular weight (HMW), middle molecular weight, and low molecular weight complexes in both human and mice. The concentration of HMW adiponectin in female was significantly higher than that in male, whereas there were no gender differences for the other two forms. Castration induced a dramatic elevation of the HMW form but had no effect on either the middle molecular weight or the low molecular weight form in mice. Testosterone treatment, on the other hand, caused a specific reduction of HMW adiponectin in the circulation. Pulse-chase labeling experiments in rat adipocytes revealed that the three oligomeric forms of adiponectin were secreted into the culture medium at different rates and that testosterone selectively impeded the secretion of HMW adiponectin but not the other two forms. The inhibitory effect of testosterone on secretion of HMW adiponectin was largely restored by the transcription inhibitor actinomycin D, suggesting the involvement of a transcriptional event in this process. The selective inhibition of HMW adiponectin by testosterone might contribute to the sex dimorphism of adiponectin in terms of its oligomeric complex distribution and could partly explain why men have higher risk to insulin resistance and atherosclerosis than women. © 2005 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/78383
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXu, Aen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorHoo, RLCen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorTan, KCBen_HK
dc.contributor.authorZhang, Jen_HK
dc.contributor.authorChen, Ben_HK
dc.contributor.authorLam, MCen_HK
dc.contributor.authorTse, Cen_HK
dc.contributor.authorCooper, GJSen_HK
dc.contributor.authorLam, KSLen_HK
dc.date.accessioned2010-09-06T07:42:16Z-
dc.date.available2010-09-06T07:42:16Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal Of Biological Chemistry, 2005, v. 280 n. 18, p. 18073-18080en_HK
dc.identifier.issn0021-9258en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78383-
dc.description.abstractThe antidiabetic hormone adiponectin circulates in blood as several oligomeric complexes, and the ratios between them are critical in determining insulin sensitivity. In this study we investigated the role of testosterone in regulating the oligomeric complex distribution of adiponectin. Gel filtration analysis revealed that circulating adiponectin existed as the forms of high molecular weight (HMW), middle molecular weight, and low molecular weight complexes in both human and mice. The concentration of HMW adiponectin in female was significantly higher than that in male, whereas there were no gender differences for the other two forms. Castration induced a dramatic elevation of the HMW form but had no effect on either the middle molecular weight or the low molecular weight form in mice. Testosterone treatment, on the other hand, caused a specific reduction of HMW adiponectin in the circulation. Pulse-chase labeling experiments in rat adipocytes revealed that the three oligomeric forms of adiponectin were secreted into the culture medium at different rates and that testosterone selectively impeded the secretion of HMW adiponectin but not the other two forms. The inhibitory effect of testosterone on secretion of HMW adiponectin was largely restored by the transcription inhibitor actinomycin D, suggesting the involvement of a transcriptional event in this process. The selective inhibition of HMW adiponectin by testosterone might contribute to the sex dimorphism of adiponectin in terms of its oligomeric complex distribution and could partly explain why men have higher risk to insulin resistance and atherosclerosis than women. © 2005 by The American Society for Biochemistry and Molecular Biology, Inc.en_HK
dc.languageengen_HK
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/en_HK
dc.relation.ispartofJournal of Biological Chemistryen_HK
dc.rightsJournal of Biological Chemistry. Copyright © American Society for Biochemistry and Molecular Biology, Inc.en_HK
dc.titleTestosterone selectively reduces the high molecular weight form of adiponectin by inhibiting its secretion from adipocytesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9258&volume=280&spage=18073&epage=80&date=2005&atitle=Testosterone+selectively+reduces+the+high+molecular+weight+form+of+adiponectin+by+inhibiting+its+secretion+from+adipocytes.en_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.emailHoo, RLC: rubyhoo@hkucc.hku.hken_HK
dc.identifier.emailWang, Y: yuwanghk@hku.hken_HK
dc.identifier.emailTan, KCB: kcbtan@hku.hken_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.identifier.authorityHoo, RLC=rp01334en_HK
dc.identifier.authorityWang, Y=rp00239en_HK
dc.identifier.authorityTan, KCB=rp00402en_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1074/jbc.M414231200en_HK
dc.identifier.scopuseid_2-s2.0-24044479055en_HK
dc.identifier.hkuros146080en_HK
dc.identifier.hkuros98181-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-24044479055&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume280en_HK
dc.identifier.issue18en_HK
dc.identifier.spage18073en_HK
dc.identifier.epage18080en_HK
dc.identifier.isiWOS:000228807200064-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK
dc.identifier.scopusauthoridChan, KW=12761148700en_HK
dc.identifier.scopusauthoridHoo, RLC=6602369766en_HK
dc.identifier.scopusauthoridWang, Y=34973733700en_HK
dc.identifier.scopusauthoridTan, KCB=8082703100en_HK
dc.identifier.scopusauthoridZhang, J=35504391800en_HK
dc.identifier.scopusauthoridChen, B=8836680100en_HK
dc.identifier.scopusauthoridLam, MC=36879143100en_HK
dc.identifier.scopusauthoridTse, C=7103295215en_HK
dc.identifier.scopusauthoridCooper, GJS=7402355946en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK

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