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Conference Paper: Toll-like receptor 4 deficiency attenuates insulin resistance and endothelial dysfunction associated with obesity and diabetes in mice

TitleToll-like receptor 4 deficiency attenuates insulin resistance and endothelial dysfunction associated with obesity and diabetes in mice
Authors
KeywordsBiology
Issue Date2010
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Experimental Biology Annual Meeting (EB 2010), Anaheim, CA., 24-28 April 2010. In The FASEB Journal, 2010, v. 24 Meeting abstract suppl., abstract no. 571.5 How to Cite?
AbstractThe present study analyzes, in mice with loss-of-function mutation of TLR4, the role of TLR4, a target for saturated fatty acids, in modulating metabolism and endothelial function. A type-2 diabetes model with double knockout (DKO) of leptin receptors (Lepr) and TLR4, was obtained by crossing Lepr(db/+) and TLR4(-/--) mice. Glucose and insulin tolerance tests were performed. Isometric tension was measured in carotid artery rings with or without endothelium. DKO mice had lower fasting serum levels of glucose, triglycerides and cholesterol and better insulin sensitivity than Lepr(db/db) control mice. Acetylcholine-induced endothelium-dependent contractions (EDCF-responses) of the carotid arteries were enhanced by genetic obesity, but were attenuated in DKO mice. They were inhibited by indomethacin and SC560, suggesting the involvement of COX-1. Apocynin, MnTMPyP, catalase, DPI, DETCA, but not deferoxamine and tiron inhibited EDCF-responses, suggesting a role for H2O2. Inhibitors including SP600128 [JNK], PD98058 [ERK] and SB203508 [MAPK] reduced the contractions in arteries of control but not of DKO mice indicating a mechanism downstream of TLR4. Rotenone and antimycin A inhibited the EDCF-response implying that mitochondria are involved. Thus, TLR4 deficiency can prevent insulin resistance and endothelial dysfunction possibly by decreasing oxidative stress in mitochondria.
DescriptionOpen Access Journal
Persistent Identifierhttp://hdl.handle.net/10722/106705
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorLiang, CFen_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-09-25T23:27:01Z-
dc.date.available2010-09-25T23:27:01Z-
dc.date.issued2010en_HK
dc.identifier.citationExperimental Biology Annual Meeting (EB 2010), Anaheim, CA., 24-28 April 2010. In The FASEB Journal, 2010, v. 24 Meeting abstract suppl., abstract no. 571.5en_HK
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/106705-
dc.descriptionOpen Access Journal-
dc.description.abstractThe present study analyzes, in mice with loss-of-function mutation of TLR4, the role of TLR4, a target for saturated fatty acids, in modulating metabolism and endothelial function. A type-2 diabetes model with double knockout (DKO) of leptin receptors (Lepr) and TLR4, was obtained by crossing Lepr(db/+) and TLR4(-/--) mice. Glucose and insulin tolerance tests were performed. Isometric tension was measured in carotid artery rings with or without endothelium. DKO mice had lower fasting serum levels of glucose, triglycerides and cholesterol and better insulin sensitivity than Lepr(db/db) control mice. Acetylcholine-induced endothelium-dependent contractions (EDCF-responses) of the carotid arteries were enhanced by genetic obesity, but were attenuated in DKO mice. They were inhibited by indomethacin and SC560, suggesting the involvement of COX-1. Apocynin, MnTMPyP, catalase, DPI, DETCA, but not deferoxamine and tiron inhibited EDCF-responses, suggesting a role for H2O2. Inhibitors including SP600128 [JNK], PD98058 [ERK] and SB203508 [MAPK] reduced the contractions in arteries of control but not of DKO mice indicating a mechanism downstream of TLR4. Rotenone and antimycin A inhibited the EDCF-response implying that mitochondria are involved. Thus, TLR4 deficiency can prevent insulin resistance and endothelial dysfunction possibly by decreasing oxidative stress in mitochondria.-
dc.languageengen_HK
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/-
dc.relation.ispartofThe FASEB Journalen_HK
dc.subjectBiology-
dc.titleToll-like receptor 4 deficiency attenuates insulin resistance and endothelial dysfunction associated with obesity and diabetes in miceen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0892-6638&volume=24, Meeting abstract suppl., abstract no. 571.5&spage=&epage=&date=2010&atitle=Toll-like+receptor+4+deficiency+attenuates+insulin+resistance+and+endothelial+dysfunction+associated+with+obesity+and+diabetes+in+mice-
dc.identifier.emailLiang, CF: chaofanliang@gmail.comen_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros170026en_HK
dc.identifier.volume24en_HK
dc.identifier.issueMeeting abstract supppl.-
dc.description.otherExperimental Biology Annual Meeting (EB 2010), Anaheim, CA., 24-28 April 2010. In The FASEB Journal, 2010, v. 24 Meeting abstract suppl., abstract no. 571.5-

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