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Article: Major urinary protein-1 increases energy expenditure and improves glucose intolerance through enhancing mitochondrial function in skeletal muscle of diabetic mice

TitleMajor urinary protein-1 increases energy expenditure and improves glucose intolerance through enhancing mitochondrial function in skeletal muscle of diabetic mice
Authors
Issue Date2009
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, 2009, v. 284 n. 21, p. 14050-14057 How to Cite?
AbstractMajor urinary protein-1 (MUP-1) is a low molecular weight secreted protein produced predominantly from the liver. Structurally it belongs to the lipocalin family, which carries small hydrophobic ligands such as pheromones. However, the physiological functions of MUP-1 remain poorly understood. Here we provide evidence demonstrating that MUP-1 is an important player in regulating energy expenditure and metabolism in mice. Both microarray and real-time PCR analysis demonstrated that the MUP-1 mRNA abundance in the liver of db/db obese mice was reduced by ∼30-fold compared with their lean littermates, whereas this change was partially reversed by treatment with the insulin-sensitizing drug rosiglitazone. In both dietary and genetic obese mice, the circulating concentrations of MUP-1 were markedly decreased compared with the lean controls. Chronic elevation of circulating MUP-1 in db/db mice, using an osmotic pump-based protein delivery system, increased energy expenditure and locomotor activity, raised core body temperature, and decreased glucose intolerance as well as insulin resistance. At the molecular level, MUP-1-mediated improvement in metabolic profiles was accompanied by increased expression of genes involved in mitochondrial biogenesis, elevated mitochondrial oxidative capacity, decreased triglyceride accumulation, and enhanced insulin-evoked Akt signaling in skeletal muscle but not in liver. Altogether, these findings raise the possibility that MUP-1 deficiency might contribute to the metabolic dysregulation in obese/diabetic mice, and suggest that the beneficial metabolic effects of MUP-1 are attributed in part to its ability in increasing mitochondrial function in skeletal muscle. © 2009 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/163258
ISSN
2014 Impact Factor: 4.573
2014 SCImago Journal Rankings: 2.734
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHui, Xen_HK
dc.contributor.authorZhu, Wen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorZhang, Jen_HK
dc.contributor.authorWu, Den_HK
dc.contributor.authorKraegen, EWen_HK
dc.contributor.authorLi, Yen_HK
dc.contributor.authorXu, Aen_HK
dc.date.accessioned2012-09-05T05:29:15Z-
dc.date.available2012-09-05T05:29:15Z-
dc.date.issued2009en_HK
dc.identifier.citationJournal Of Biological Chemistry, 2009, v. 284 n. 21, p. 14050-14057en_HK
dc.identifier.issn0021-9258en_HK
dc.identifier.urihttp://hdl.handle.net/10722/163258-
dc.description.abstractMajor urinary protein-1 (MUP-1) is a low molecular weight secreted protein produced predominantly from the liver. Structurally it belongs to the lipocalin family, which carries small hydrophobic ligands such as pheromones. However, the physiological functions of MUP-1 remain poorly understood. Here we provide evidence demonstrating that MUP-1 is an important player in regulating energy expenditure and metabolism in mice. Both microarray and real-time PCR analysis demonstrated that the MUP-1 mRNA abundance in the liver of db/db obese mice was reduced by ∼30-fold compared with their lean littermates, whereas this change was partially reversed by treatment with the insulin-sensitizing drug rosiglitazone. In both dietary and genetic obese mice, the circulating concentrations of MUP-1 were markedly decreased compared with the lean controls. Chronic elevation of circulating MUP-1 in db/db mice, using an osmotic pump-based protein delivery system, increased energy expenditure and locomotor activity, raised core body temperature, and decreased glucose intolerance as well as insulin resistance. At the molecular level, MUP-1-mediated improvement in metabolic profiles was accompanied by increased expression of genes involved in mitochondrial biogenesis, elevated mitochondrial oxidative capacity, decreased triglyceride accumulation, and enhanced insulin-evoked Akt signaling in skeletal muscle but not in liver. Altogether, these findings raise the possibility that MUP-1 deficiency might contribute to the metabolic dysregulation in obese/diabetic mice, and suggest that the beneficial metabolic effects of MUP-1 are attributed in part to its ability in increasing mitochondrial function in skeletal muscle. © 2009 by The American Society for Biochemistry and Molecular Biology, Inc.en_HK
dc.languageengen_US
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.-
dc.subject.meshAnimalsen_US
dc.subject.meshDiabetes Mellitus, Experimental - Complications - Enzymology - Physiopathologyen_US
dc.subject.meshDietary Fats - Administration & Dosage - Pharmacologyen_US
dc.subject.meshEnergy Metabolism - Drug Effectsen_US
dc.subject.meshFeeding Behavior - Drug Effectsen_US
dc.subject.meshGlucose Intolerance - Complications - Physiopathologyen_US
dc.subject.meshInsulin - Pharmacologyen_US
dc.subject.meshInsulin Resistanceen_US
dc.subject.meshLipid Metabolism - Drug Effectsen_US
dc.subject.meshLiver - Drug Effects - Metabolism - Physiopathologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57blen_US
dc.subject.meshMice, Obeseen_US
dc.subject.meshMitochondria - Drug Effects - Metabolismen_US
dc.subject.meshMotor Activity - Drug Effectsen_US
dc.subject.meshMuscle, Skeletal - Drug Effects - Enzymology - Physiopathologyen_US
dc.subject.meshProteins - Metabolismen_US
dc.subject.meshProto-Oncogene Proteins C-Akt - Metabolismen_US
dc.subject.meshRecombinant Proteins - Administration & Dosage - Pharmacologyen_US
dc.subject.meshSignal Transduction - Drug Effectsen_US
dc.subject.meshThiazolidinediones - Pharmacologyen_US
dc.subject.meshUp-Regulation - Drug Effectsen_US
dc.titleMajor urinary protein-1 increases energy expenditure and improves glucose intolerance through enhancing mitochondrial function in skeletal muscle of diabetic miceen_HK
dc.typeArticleen_HK
dc.identifier.emailWang, Y: yuwanghk@hku.hken_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.authorityWang, Y=rp00239en_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1074/jbc.M109.001107en_HK
dc.identifier.pmid19336396en_HK
dc.identifier.scopuseid_2-s2.0-67649774119en_HK
dc.identifier.hkuros157898-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67649774119&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume284en_HK
dc.identifier.issue21en_HK
dc.identifier.spage14050en_HK
dc.identifier.epage14057en_HK
dc.identifier.isiWOS:000266286100011-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHui, X=26666795900en_HK
dc.identifier.scopusauthoridZhu, W=7404232544en_HK
dc.identifier.scopusauthoridWang, Y=34973733700en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK
dc.identifier.scopusauthoridZhang, J=35504391800en_HK
dc.identifier.scopusauthoridWu, D=7404297751en_HK
dc.identifier.scopusauthoridKraegen, EW=7006873142en_HK
dc.identifier.scopusauthoridLi, Y=9274991700en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK
dc.identifier.citeulike6416774-

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