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Article: Type 2 diabetes mellitus and endothelial lipase

TitleType 2 diabetes mellitus and endothelial lipase
Authors
Issue Date2008
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis
Citation
Atherosclerosis, 2008, v. 198 n. 2, p. 441-447 How to Cite?
AbstractObjective: Endothelial lipase (EL), a new member of the triacylglycerol lipase family, modulates the metabolism of high-density lipoproteins and is upregulated by inflammatory cytokines. Since type 2 diabetes is associated with chronic subclinical inflammation, we have determined whether serum EL concentration is increased in type 2 diabetes and investigated the effect of insulin on EL. Methods: 237 type 2 diabetic patients on oral anti-diabetic agents, 111 type 2 diabetic patients on insulin therapy and 226 non-diabetic controls were recruited. Serum EL was measured by ELISA. To investigate the effect of insulin on EL production by endothelial cells, human aortic endothelial cells were incubated with insulin and EL mRNA and protein in cell medium was measured. Serum EL was also measured in 16 diabetic subjects before and after starting insulin therapy. Results: Serum EL level was highest in patients on oral anti-diabetic agents whereas those on insulin had similar EL level as controls (oral: 26.7 ± 16.1 ng/ml; insulin: 23.3 ± 11.6, controls: 23.9 ± 12.0; ANOVA p = 0.04). In both controls and patients on oral anti-diabetic agents, EL correlated with log(CRP) (r = 0.20, p = 0.003; r = 0.23, p < 0.001, respectively) but no correlation was seen in patients on insulin. In vitro experiments showed that insulin significantly reduced EL mRNA and protein in human aortic endothelial cells in a dose-dependent manner. Serum EL concentration also significantly decreased in diabetic patients after starting insulin therapy (p < 0.03). Conclusion: Serum EL concentration was increased in type 2 diabetic patients and was associated with the degree of subclinical inflammation and exogenous insulin therapy lowered serum EL concentration. © 2008 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/77949
ISSN
2015 Impact Factor: 3.942
2015 SCImago Journal Rankings: 1.819
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShiu, SWMen_HK
dc.contributor.authorTan, KCBen_HK
dc.contributor.authorHuang, Yen_HK
dc.contributor.authorWong, Yen_HK
dc.date.accessioned2010-09-06T07:37:31Z-
dc.date.available2010-09-06T07:37:31Z-
dc.date.issued2008en_HK
dc.identifier.citationAtherosclerosis, 2008, v. 198 n. 2, p. 441-447en_HK
dc.identifier.issn0021-9150en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77949-
dc.description.abstractObjective: Endothelial lipase (EL), a new member of the triacylglycerol lipase family, modulates the metabolism of high-density lipoproteins and is upregulated by inflammatory cytokines. Since type 2 diabetes is associated with chronic subclinical inflammation, we have determined whether serum EL concentration is increased in type 2 diabetes and investigated the effect of insulin on EL. Methods: 237 type 2 diabetic patients on oral anti-diabetic agents, 111 type 2 diabetic patients on insulin therapy and 226 non-diabetic controls were recruited. Serum EL was measured by ELISA. To investigate the effect of insulin on EL production by endothelial cells, human aortic endothelial cells were incubated with insulin and EL mRNA and protein in cell medium was measured. Serum EL was also measured in 16 diabetic subjects before and after starting insulin therapy. Results: Serum EL level was highest in patients on oral anti-diabetic agents whereas those on insulin had similar EL level as controls (oral: 26.7 ± 16.1 ng/ml; insulin: 23.3 ± 11.6, controls: 23.9 ± 12.0; ANOVA p = 0.04). In both controls and patients on oral anti-diabetic agents, EL correlated with log(CRP) (r = 0.20, p = 0.003; r = 0.23, p < 0.001, respectively) but no correlation was seen in patients on insulin. In vitro experiments showed that insulin significantly reduced EL mRNA and protein in human aortic endothelial cells in a dose-dependent manner. Serum EL concentration also significantly decreased in diabetic patients after starting insulin therapy (p < 0.03). Conclusion: Serum EL concentration was increased in type 2 diabetic patients and was associated with the degree of subclinical inflammation and exogenous insulin therapy lowered serum EL concentration. © 2008 Elsevier Ireland Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosisen_HK
dc.relation.ispartofAtherosclerosisen_HK
dc.rightsAtherosclerosis . Copyright © Elsevier Ireland Ltd.en_HK
dc.subject.meshAdulten_HK
dc.subject.meshAorta - enzymologyen_HK
dc.subject.meshDiabetes Mellitus, Type 2 - diagnosis - drug therapyen_HK
dc.subject.meshEndothelium, Vascular - enzymologyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshHypoglycemic Agents - administration & dosage - therapeutic useen_HK
dc.subject.meshInsulin - administration & dosage - therapeutic useen_HK
dc.subject.meshLipase - blood - genetics - metabolismen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshRNA, Messenger - analysis - metabolismen_HK
dc.titleType 2 diabetes mellitus and endothelial lipaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9150&volume=198&spage=441&epage=7&date=2008&atitle=Type+2+diabetes+mellitus+and+endothelial+lipaseen_HK
dc.identifier.emailTan, KCB:kcbtan@hku.hken_HK
dc.identifier.authorityTan, KCB=rp00402en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.atherosclerosis.2008.03.012en_HK
dc.identifier.pmid18433755-
dc.identifier.scopuseid_2-s2.0-43949126841en_HK
dc.identifier.hkuros145703en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-43949126841&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume198en_HK
dc.identifier.issue2en_HK
dc.identifier.spage441en_HK
dc.identifier.epage447en_HK
dc.identifier.isiWOS:000257133600027-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridShiu, SWM=7005550652en_HK
dc.identifier.scopusauthoridTan, KCB=8082703100en_HK
dc.identifier.scopusauthoridHuang, Y=34770915100en_HK
dc.identifier.scopusauthoridWong, Y=24073787400en_HK

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