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Article: Rosiglitazone ameliorates abnormal expression and activity of protein tyrosine phosphatase 1B in the skeletal muscle of fat-fed, streptozotocin- treated diabetic rats

TitleRosiglitazone ameliorates abnormal expression and activity of protein tyrosine phosphatase 1B in the skeletal muscle of fat-fed, streptozotocin- treated diabetic rats
Authors
Issue Date2005
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 2005, v. 146 n. 2, p. 234-243 How to Cite?
AbstractProtein tyrosine phosphatase 1B (PTP1B) acts as a physiological negative regulator of insulin signaling by dephosphorylating the activated insulin receptor (IR). Here we examine the role of PTP1B in the insulin-sensitizing action of rosiglitazone (RSG) in skeletal muscle and liver. Fat-fed, streptozotocin-treated rats (10-week-old), an animal model of type II diabetes, and age-matched, nondiabetic controls were treated with RSG (10 μumol kg -1 day -1) for 2 weeks. After RSG treatment, the diabetic rats showed a significant decrease in blood glucose and improved insulin sensitivity. Diabetic rats showed significantly increased levels and activities of PTP1B in the skeletal muscle (1.6- and 2-fold, respectively) and liver (1.7- and 1.8-fold, respectively), thus diminishing insulin signaling in the target tissues. We found that the decreases in insulin-stimulated glucose uptake (55%), tyrosine phosphorylation of IRβ-subunits (48%), and IR substrate-1 (IRS-1) (39%) in muscles of diabetic rats were normalized after RSG treatment. These effects were associated with 34 and 30% decreases in increased PTP1B levels and activities, respectively, in skeletal muscles of diabetic rats. In contrast, RSG did not affect the increased PTP1B levels and activities or the already reduced insulin-stimulated glycogen synthesis and tyrosine phosphorylation of IRβ-subunits and IRS-2 in livers of diabetic rats. RSG treatment in normal rats did not significantly change PTP1B activities and levels or protein levels of IRβ, IRS-1, and -2 in diabetic rats. These data suggest that RSG enhances insulin activity in skeletal muscle of diabetic rats possibly by ameliorating abnormal levels and activities of PTP1B. © 2005 Nature Publishing Group All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/147225
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWu, Yen_US
dc.contributor.authorOuyang, JPen_US
dc.contributor.authorWu, Ken_US
dc.contributor.authorWang, SSen_US
dc.contributor.authorWen, CYen_US
dc.contributor.authorXia, ZYen_US
dc.date.accessioned2012-05-29T06:00:54Z-
dc.date.available2012-05-29T06:00:54Z-
dc.date.issued2005en_US
dc.identifier.citationBritish Journal Of Pharmacology, 2005, v. 146 n. 2, p. 234-243en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/147225-
dc.description.abstractProtein tyrosine phosphatase 1B (PTP1B) acts as a physiological negative regulator of insulin signaling by dephosphorylating the activated insulin receptor (IR). Here we examine the role of PTP1B in the insulin-sensitizing action of rosiglitazone (RSG) in skeletal muscle and liver. Fat-fed, streptozotocin-treated rats (10-week-old), an animal model of type II diabetes, and age-matched, nondiabetic controls were treated with RSG (10 μumol kg -1 day -1) for 2 weeks. After RSG treatment, the diabetic rats showed a significant decrease in blood glucose and improved insulin sensitivity. Diabetic rats showed significantly increased levels and activities of PTP1B in the skeletal muscle (1.6- and 2-fold, respectively) and liver (1.7- and 1.8-fold, respectively), thus diminishing insulin signaling in the target tissues. We found that the decreases in insulin-stimulated glucose uptake (55%), tyrosine phosphorylation of IRβ-subunits (48%), and IR substrate-1 (IRS-1) (39%) in muscles of diabetic rats were normalized after RSG treatment. These effects were associated with 34 and 30% decreases in increased PTP1B levels and activities, respectively, in skeletal muscles of diabetic rats. In contrast, RSG did not affect the increased PTP1B levels and activities or the already reduced insulin-stimulated glycogen synthesis and tyrosine phosphorylation of IRβ-subunits and IRS-2 in livers of diabetic rats. RSG treatment in normal rats did not significantly change PTP1B activities and levels or protein levels of IRβ, IRS-1, and -2 in diabetic rats. These data suggest that RSG enhances insulin activity in skeletal muscle of diabetic rats possibly by ameliorating abnormal levels and activities of PTP1B. © 2005 Nature Publishing Group All rights reserved.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_US
dc.relation.ispartofBritish Journal of Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshDiabetes Mellitus, Experimental - Enzymologyen_US
dc.subject.meshDiabetes Mellitus, Type 2 - Chemically Induced - Metabolismen_US
dc.subject.meshDietary Fats - Pharmacologyen_US
dc.subject.meshGlucose - Metabolismen_US
dc.subject.meshGlucose Tolerance Testen_US
dc.subject.meshGlycogen - Biosynthesisen_US
dc.subject.meshHepatocytes - Drug Effects - Metabolismen_US
dc.subject.meshHypoglycemic Agents - Pharmacologyen_US
dc.subject.meshInsulin - Metabolismen_US
dc.subject.meshInsulin Resistanceen_US
dc.subject.meshLiver - Drug Effects - Metabolism - Physiologyen_US
dc.subject.meshLiver Glycogen - Biosynthesisen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle, Skeletal - Drug Effects - Enzymology - Metabolism - Physiologyen_US
dc.subject.meshProtein Tyrosine Phosphatase, Non-Receptor Type 1en_US
dc.subject.meshProtein Tyrosine Phosphatases - Biosynthesisen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshSignal Transduction - Drug Effectsen_US
dc.subject.meshThiazolidinediones - Pharmacologyen_US
dc.titleRosiglitazone ameliorates abnormal expression and activity of protein tyrosine phosphatase 1B in the skeletal muscle of fat-fed, streptozotocin- treated diabetic ratsen_US
dc.typeArticleen_US
dc.identifier.emailXia, ZY:zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, ZY=rp00532en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.bjp.0706306en_US
dc.identifier.pmid15997237en_US
dc.identifier.scopuseid_2-s2.0-30544435421en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-30544435421&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume146en_US
dc.identifier.issue2en_US
dc.identifier.spage234en_US
dc.identifier.epage243en_US
dc.identifier.isiWOS:000232317100010-
dc.publisher.placeUnited Kingdomen_US

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