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Article: Adiponectin Ameliorates Dyslipidemia Induced by the Human Immunodeficiency Virus Protease Inhibitor Ritonavir in Mice

TitleAdiponectin Ameliorates Dyslipidemia Induced by the Human Immunodeficiency Virus Protease Inhibitor Ritonavir in Mice
Authors
Issue Date2004
PublisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.org
Citation
Endocrinology, 2004, v. 145 n. 2, p. 487-494 How to Cite?
AbstractAlthough the clinical application of HIV protease inhibitors (PIs) has markedly reduced HIV-related morbidity and mortality, it is now recognized that PI-based therapy often causes serious metabolic disorders, including hyperlipidemia and premature atherosclerosis. The etiology of these adverse effects remains obscure. Here, we demonstrate that deficiency of the fat-derived hormone adiponectin might play a role. The steady-state mRNA levels of the adiponectin gene and secretion of this protein from 3T3-L1 adipocytes are significantly decreased after treatment with several PIs (indinavir, nelfinavir, and ritonavir), with ritonavir having the greatest effect. Intragastric administration of ritonavir into mice decreases plasma concentrations of adiponectin and concurrently increases the plasma levels of triglyceride, free fatty acids, and cholesterol. Adiponectin replacement therapy markedly ameliorates ritonavir-induced elevations of triglyceride and free fatty acids. These beneficial effects of adiponectin are partly due to its ability to decrease ritonavir-induced synthesis of fatty acids and triglyceride, and to increase fatty acid combustion in the liver tissue. In contrast, adiponectin has little effect on ritonavir-induced hypercholesterolemia and hepatic cholesterol synthesis. These results suggest that hypoadiponectinemia is partly responsible for the metabolic disorders induced by HIV PIs, and adiponectin or its agonists might be useful for the treatment of these disorders.
Persistent Identifierhttp://hdl.handle.net/10722/76690
ISSN
2015 Impact Factor: 4.159
2015 SCImago Journal Rankings: 2.363
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXu, Aen_HK
dc.contributor.authorYin, Sen_HK
dc.contributor.authorWong, Len_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorLam, KSLen_HK
dc.date.accessioned2010-09-06T07:23:54Z-
dc.date.available2010-09-06T07:23:54Z-
dc.date.issued2004en_HK
dc.identifier.citationEndocrinology, 2004, v. 145 n. 2, p. 487-494en_HK
dc.identifier.issn0013-7227en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76690-
dc.description.abstractAlthough the clinical application of HIV protease inhibitors (PIs) has markedly reduced HIV-related morbidity and mortality, it is now recognized that PI-based therapy often causes serious metabolic disorders, including hyperlipidemia and premature atherosclerosis. The etiology of these adverse effects remains obscure. Here, we demonstrate that deficiency of the fat-derived hormone adiponectin might play a role. The steady-state mRNA levels of the adiponectin gene and secretion of this protein from 3T3-L1 adipocytes are significantly decreased after treatment with several PIs (indinavir, nelfinavir, and ritonavir), with ritonavir having the greatest effect. Intragastric administration of ritonavir into mice decreases plasma concentrations of adiponectin and concurrently increases the plasma levels of triglyceride, free fatty acids, and cholesterol. Adiponectin replacement therapy markedly ameliorates ritonavir-induced elevations of triglyceride and free fatty acids. These beneficial effects of adiponectin are partly due to its ability to decrease ritonavir-induced synthesis of fatty acids and triglyceride, and to increase fatty acid combustion in the liver tissue. In contrast, adiponectin has little effect on ritonavir-induced hypercholesterolemia and hepatic cholesterol synthesis. These results suggest that hypoadiponectinemia is partly responsible for the metabolic disorders induced by HIV PIs, and adiponectin or its agonists might be useful for the treatment of these disorders.en_HK
dc.languageengen_HK
dc.publisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.orgen_HK
dc.relation.ispartofEndocrinologyen_HK
dc.rightsEndocrinology . Copyright © The Endocrine Society.en_HK
dc.subject.mesh3T3 Cellsen_HK
dc.subject.meshAdipocytes - metabolismen_HK
dc.subject.meshAdiponectinen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBlotting, Northernen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshCholesterol - biosynthesis - blooden_HK
dc.subject.meshDose-Response Relationship, Drugen_HK
dc.subject.meshFatty Acids - metabolismen_HK
dc.subject.meshFatty Acids, Nonesterified - blooden_HK
dc.subject.meshGene Expression - drug effectsen_HK
dc.subject.meshHIV Protease Inhibitors - adverse effects - pharmacologyen_HK
dc.subject.meshHormone Replacement Therapyen_HK
dc.subject.meshHyperlipidemias - chemically induceden_HK
dc.subject.meshIntercellular Signaling Peptides and Proteinsen_HK
dc.subject.meshLiver - metabolismen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshOxidation-Reductionen_HK
dc.subject.meshProteins - genetics - physiology - therapeutic useen_HK
dc.subject.meshRecombinant Proteins - therapeutic useen_HK
dc.subject.meshRitonavir - adverse effects - pharmacologyen_HK
dc.subject.meshTriglycerides - biosynthesis - blooden_HK
dc.titleAdiponectin Ameliorates Dyslipidemia Induced by the Human Immunodeficiency Virus Protease Inhibitor Ritonavir in Miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0013-7227&volume=145&spage=487&epage=94&date=2004&atitle=Adiponectin+ameliorates+dyslipidemia+induced+by+the+human+immunodeficiency+virus+protease+inhibitor+ritonavir+in+miceen_HK
dc.identifier.emailXu, A:amxu@hkucc.hku.hken_HK
dc.identifier.emailLam, KSL:ksllam@hku.hken_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1210/en.2003-1140en_HK
dc.identifier.pmid14592951en_HK
dc.identifier.scopuseid_2-s2.0-0842291596en_HK
dc.identifier.hkuros91084en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0842291596&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume145en_HK
dc.identifier.issue2en_HK
dc.identifier.spage487en_HK
dc.identifier.epage494en_HK
dc.identifier.isiWOS:000188304400006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK
dc.identifier.scopusauthoridYin, S=8979453800en_HK
dc.identifier.scopusauthoridWong, L=25123484000en_HK
dc.identifier.scopusauthoridChan, KW=12761148700en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK

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