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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
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TitleMajor urinary protein-1 increases energy expenditure and improves glucose intolerance through enhancing mitochondrial function in skeletal muscle of diabetic mice
 
AuthorsHui, X1
Zhu, W2
Wang, Y2
Lam, KSL2
Zhang, J2
Wu, D3
Kraegen, EW4
Li, Y1
Xu, A2
 
Issue Date2009
 
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
 
CitationJournal Of Biological Chemistry, 2009, v. 284 n. 21, p. 14050-14057 [How to Cite?]
DOI: http://dx.doi.org/10.1074/jbc.M109.001107
 
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.
 
ISSN0021-9258
2013 Impact Factor: 4.600
 
DOIhttp://dx.doi.org/10.1074/jbc.M109.001107
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorHui, X
 
dc.contributor.authorZhu, W
 
dc.contributor.authorWang, Y
 
dc.contributor.authorLam, KSL
 
dc.contributor.authorZhang, J
 
dc.contributor.authorWu, D
 
dc.contributor.authorKraegen, EW
 
dc.contributor.authorLi, Y
 
dc.contributor.authorXu, A
 
dc.date.accessioned2012-09-05T05:29:15Z
 
dc.date.available2012-09-05T05:29:15Z
 
dc.date.issued2009
 
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.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationJournal Of Biological Chemistry, 2009, v. 284 n. 21, p. 14050-14057 [How to Cite?]
DOI: http://dx.doi.org/10.1074/jbc.M109.001107
 
dc.identifier.citeulike6416774
 
dc.identifier.doihttp://dx.doi.org/10.1074/jbc.M109.001107
 
dc.identifier.epage14057
 
dc.identifier.hkuros157898
 
dc.identifier.issn0021-9258
2013 Impact Factor: 4.600
 
dc.identifier.issue21
 
dc.identifier.pmid19336396
 
dc.identifier.scopuseid_2-s2.0-67649774119
 
dc.identifier.spage14050
 
dc.identifier.urihttp://hdl.handle.net/10722/163258
 
dc.identifier.volume284
 
dc.languageeng
 
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofJournal of Biological Chemistry
 
dc.relation.referencesReferences in Scopus
 
dc.rightsJournal of Biological Chemistry. Copyright © American Society for Biochemistry and Molecular Biology, Inc.
 
dc.subject.meshAnimals
 
dc.subject.meshDiabetes Mellitus, Experimental - Complications - Enzymology - Physiopathology
 
dc.subject.meshDietary Fats - Administration & Dosage - Pharmacology
 
dc.subject.meshEnergy Metabolism - Drug Effects
 
dc.subject.meshFeeding Behavior - Drug Effects
 
dc.subject.meshGlucose Intolerance - Complications - Physiopathology
 
dc.subject.meshInsulin - Pharmacology
 
dc.subject.meshInsulin Resistance
 
dc.subject.meshLipid Metabolism - Drug Effects
 
dc.subject.meshLiver - Drug Effects - Metabolism - Physiopathology
 
dc.subject.meshMice
 
dc.subject.meshMice, Inbred C57bl
 
dc.subject.meshMice, Obese
 
dc.subject.meshMitochondria - Drug Effects - Metabolism
 
dc.subject.meshMotor Activity - Drug Effects
 
dc.subject.meshMuscle, Skeletal - Drug Effects - Enzymology - Physiopathology
 
dc.subject.meshProteins - Metabolism
 
dc.subject.meshProto-Oncogene Proteins C-Akt - Metabolism
 
dc.subject.meshRecombinant Proteins - Administration & Dosage - Pharmacology
 
dc.subject.meshSignal Transduction - Drug Effects
 
dc.subject.meshThiazolidinediones - Pharmacology
 
dc.subject.meshUp-Regulation - Drug Effects
 
dc.titleMajor urinary protein-1 increases energy expenditure and improves glucose intolerance through enhancing mitochondrial function in skeletal muscle of diabetic mice
 
dc.typeArticle
 
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Author Affiliations
  1. Graduate University of Chinese Academy of Sciences
  2. The University of Hong Kong
  3. Chinese Academy of Sciences
  4. University of New South Wales