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Article: Comparison of vascular relaxation, lipolysis and glucose uptake by peroxisome proliferator-activated receptor-γ activation in + db/+ m and + db/+ db mice

TitleComparison of vascular relaxation, lipolysis and glucose uptake by peroxisome proliferator-activated receptor-γ activation in + db/+ m and + db/+ db mice
Authors
Keywords+ db/+ db mice
Aortic relaxation
Glucose uptake
Lipolysis
Peroxisome proliferator-activated receptor-γ
Issue Date2007
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejphar
Citation
European Journal Of Pharmacology, 2007, v. 572 n. 1, p. 40-48 How to Cite?
Abstract
In this study, we determined the in vitro effect of peroxisome proliferator-activated receptor-γ (PPAR-γ) activation on the aortic relaxation, lipolysis and insulin-induced [ 3H]-glucose uptake of the abdominal (omental) adipocytes of the non-diabetic (+ db/+ m) and obese/diabetic (+ db/+ db) mice. The expression of PPAR-γ (mRNA and protein) in aorta and adipose tissues was evaluated and compared. Cumulative application of ciglitazone, pioglitazone and troglitazone (PPAR-γ agonists) caused a concentration-dependent aortic relaxation (sensitive to 2-chloro-5-nitro-N-phenylbenzamide (GW9662) (1 μM, a selective PPAR-γ antagonist) and N ω-nitro-l-arginine methyl ester (l-NAME) (20 μM, a nitric oxide synthase inhibitor)) with a maximum relaxation of ∼ 30% (3 μM) in + db/+ m mice, whereas no relaxation was observed in + db/+ db mice. All PPAR-γ agonists examined did not alter the basal lipolysis of both species, but forskolin caused a concentration-dependent lipolysis, with a greater magnitude observed in + db/+ m mice. Insulin (0.1 and 1 μM) caused an enhancement of [ 3H]-glucose uptake into adipocytes with a greater magnitude in + db/+ m mice. In contrast, none of the PPAR-γ agonists tested (0.1, 1 and 10 μM) altered the basal and the insulin (0.1 μM)-induced [ 3H]-glucose uptake into adipocytes of both species. In addition, there was no difference in PPAR-γ expression (mRNA and protein) in the aorta and adipose tissues between the species. In conclusion, our results demonstrate that PPAR-γ is present in the abdominal (omental) adipose tissue and thoracic aorta. An acute activation of PPAR-γ produced a small (∼ 30%) aortic relaxation (nitric oxide/endothelium-dependent) of + db/+ m mice. However, all PPAR-γ agonists examined have no acute effect on lipolysis and the insulin-induced glucose uptake into adipocytes of both + db/+ m and + db/+ db mice. © 2007 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/80326
ISSN
2013 Impact Factor: 2.684
2013 SCImago Journal Rankings: 1.067
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSeto, SWen_HK
dc.contributor.authorLam, TYen_HK
dc.contributor.authorLeung, GPHen_HK
dc.contributor.authorAu, ALSen_HK
dc.contributor.authorNgai, SMen_HK
dc.contributor.authorChan, SWen_HK
dc.contributor.authorKwan, YWen_HK
dc.date.accessioned2010-09-06T08:05:04Z-
dc.date.available2010-09-06T08:05:04Z-
dc.date.issued2007en_HK
dc.identifier.citationEuropean Journal Of Pharmacology, 2007, v. 572 n. 1, p. 40-48en_HK
dc.identifier.issn0014-2999en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80326-
dc.description.abstractIn this study, we determined the in vitro effect of peroxisome proliferator-activated receptor-γ (PPAR-γ) activation on the aortic relaxation, lipolysis and insulin-induced [ 3H]-glucose uptake of the abdominal (omental) adipocytes of the non-diabetic (+ db/+ m) and obese/diabetic (+ db/+ db) mice. The expression of PPAR-γ (mRNA and protein) in aorta and adipose tissues was evaluated and compared. Cumulative application of ciglitazone, pioglitazone and troglitazone (PPAR-γ agonists) caused a concentration-dependent aortic relaxation (sensitive to 2-chloro-5-nitro-N-phenylbenzamide (GW9662) (1 μM, a selective PPAR-γ antagonist) and N ω-nitro-l-arginine methyl ester (l-NAME) (20 μM, a nitric oxide synthase inhibitor)) with a maximum relaxation of ∼ 30% (3 μM) in + db/+ m mice, whereas no relaxation was observed in + db/+ db mice. All PPAR-γ agonists examined did not alter the basal lipolysis of both species, but forskolin caused a concentration-dependent lipolysis, with a greater magnitude observed in + db/+ m mice. Insulin (0.1 and 1 μM) caused an enhancement of [ 3H]-glucose uptake into adipocytes with a greater magnitude in + db/+ m mice. In contrast, none of the PPAR-γ agonists tested (0.1, 1 and 10 μM) altered the basal and the insulin (0.1 μM)-induced [ 3H]-glucose uptake into adipocytes of both species. In addition, there was no difference in PPAR-γ expression (mRNA and protein) in the aorta and adipose tissues between the species. In conclusion, our results demonstrate that PPAR-γ is present in the abdominal (omental) adipose tissue and thoracic aorta. An acute activation of PPAR-γ produced a small (∼ 30%) aortic relaxation (nitric oxide/endothelium-dependent) of + db/+ m mice. However, all PPAR-γ agonists examined have no acute effect on lipolysis and the insulin-induced glucose uptake into adipocytes of both + db/+ m and + db/+ db mice. © 2007 Elsevier B.V. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejpharen_HK
dc.relation.ispartofEuropean Journal of Pharmacologyen_HK
dc.rightsEuropean Journal of Pharmacology. Copyright © Elsevier BV.en_HK
dc.subject+ db/+ db miceen_HK
dc.subjectAortic relaxationen_HK
dc.subjectGlucose uptakeen_HK
dc.subjectLipolysisen_HK
dc.subjectPeroxisome proliferator-activated receptor-γen_HK
dc.titleComparison of vascular relaxation, lipolysis and glucose uptake by peroxisome proliferator-activated receptor-γ activation in + db/+ m and + db/+ db miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0014-2999&volume=572&spage=40&epage=48&date=2007&atitle=Comparison+of+vascular+relaxation,+lipolysis+and+glucose+uptake+by+peroxisome+proliferator-activated+receptor-gamma+activation+in++db/+m+and++db/+db+miceen_HK
dc.identifier.emailLeung, GPH: gphleung@hkucc.hku.hken_HK
dc.identifier.authorityLeung, GPH=rp00234en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.ejphar.2007.05.070en_HK
dc.identifier.pmid17603034en_HK
dc.identifier.scopuseid_2-s2.0-34548495791en_HK
dc.identifier.hkuros157509en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34548495791&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume572en_HK
dc.identifier.issue1en_HK
dc.identifier.spage40en_HK
dc.identifier.epage48en_HK
dc.identifier.isiWOS:000250191200005-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridSeto, SW=9941482400en_HK
dc.identifier.scopusauthoridLam, TY=18134321000en_HK
dc.identifier.scopusauthoridLeung, GPH=35963668200en_HK
dc.identifier.scopusauthoridAu, ALS=7005391144en_HK
dc.identifier.scopusauthoridNgai, SM=7006074219en_HK
dc.identifier.scopusauthoridChan, SW=7404255670en_HK
dc.identifier.scopusauthoridKwan, YW=7005662153en_HK

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