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Article: Endothelial lipase and reverse cholesterol transport in type 2 diabetes mellitus

TitleEndothelial lipase and reverse cholesterol transport in type 2 diabetes mellitus
Authors
KeywordsCholesterol efflux
Endothelial lipase
Reverse cholesterol transport
Issue Date2010
PublisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=2040-1116&site=1
Citation
Journal Of Diabetes Investigation, 2010, v. 1 n. 3, p. 111-116 How to Cite?
AbstractAims/Introduction: Endothelial lipase (EL) plays an important role in high-density lipoprotein (HDL) metabolism and experimental data suggest that EL might be proatherogenic. We have investigated whether serum EL concentration is associated with changes in serum capacity to induce cholesterol efflux and arterial stiffness in type 2 diabetes. Materials and Methods: Serum EL was assayed by ELISA in 172 diabetic patients and 175 controls. The ability of serum to induce cholesterol efflux was measured using a cell culture system and arterial stiffness was determined by measuring pulse wave velocity (PWV) between carotid and femoral arteries. Results: Diabetic patients had significantly higher C-reactive protein (CRP) and EL (27.7 ± 16.6 ng/mL vs 24.0 ± 11.3, P < 0.05). Cholesterol efflux to serum mediated through scavenger receptor class B type I was impaired (15.1 ± 2.5% vs 16.7 ± 3.1, respectively, P < 0.01). In controls, serum EL correlated with cholesterol efflux to serum (r =)0.16, P = 0.025), but only a trend was seen in the diabetic patients. Linear regression showed that in controls, HDL, serum EL and waist circumference were major independent determinants of cholesterol efflux; whereas in the diabetic cohort, the major independent determinants of cholesterol efflux were HDL, CRP and age. PWV was increased in the diabetic patients (P < 0.01), but no association between serum EL and PWV was seen in either groups. Conclusions: Serum EL was increased in diabetic patients, but impaired serum capacity to induce cholesterol efflux in these patients was mainly related to low HDL and subclinical inflammation. © 2010 Asian Association for the Study of Diabetes and Blackwell Publishing Asia Pty Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/125041
ISSN
2021 Impact Factor: 3.681
2020 SCImago Journal Rankings: 1.089
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShiu, SWMen_HK
dc.contributor.authorZhou, Hen_HK
dc.contributor.authorWong, Yen_HK
dc.contributor.authorTan, KCBen_HK
dc.date.accessioned2010-10-31T11:08:09Z-
dc.date.available2010-10-31T11:08:09Z-
dc.date.issued2010en_HK
dc.identifier.citationJournal Of Diabetes Investigation, 2010, v. 1 n. 3, p. 111-116en_HK
dc.identifier.issn2040-1116en_HK
dc.identifier.urihttp://hdl.handle.net/10722/125041-
dc.description.abstractAims/Introduction: Endothelial lipase (EL) plays an important role in high-density lipoprotein (HDL) metabolism and experimental data suggest that EL might be proatherogenic. We have investigated whether serum EL concentration is associated with changes in serum capacity to induce cholesterol efflux and arterial stiffness in type 2 diabetes. Materials and Methods: Serum EL was assayed by ELISA in 172 diabetic patients and 175 controls. The ability of serum to induce cholesterol efflux was measured using a cell culture system and arterial stiffness was determined by measuring pulse wave velocity (PWV) between carotid and femoral arteries. Results: Diabetic patients had significantly higher C-reactive protein (CRP) and EL (27.7 ± 16.6 ng/mL vs 24.0 ± 11.3, P < 0.05). Cholesterol efflux to serum mediated through scavenger receptor class B type I was impaired (15.1 ± 2.5% vs 16.7 ± 3.1, respectively, P < 0.01). In controls, serum EL correlated with cholesterol efflux to serum (r =)0.16, P = 0.025), but only a trend was seen in the diabetic patients. Linear regression showed that in controls, HDL, serum EL and waist circumference were major independent determinants of cholesterol efflux; whereas in the diabetic cohort, the major independent determinants of cholesterol efflux were HDL, CRP and age. PWV was increased in the diabetic patients (P < 0.01), but no association between serum EL and PWV was seen in either groups. Conclusions: Serum EL was increased in diabetic patients, but impaired serum capacity to induce cholesterol efflux in these patients was mainly related to low HDL and subclinical inflammation. © 2010 Asian Association for the Study of Diabetes and Blackwell Publishing Asia Pty Ltd.en_HK
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=2040-1116&site=1en_HK
dc.relation.ispartofJournal of Diabetes Investigationen_HK
dc.rightsThe definitive version is available at www3.interscience.wiley.com-
dc.subjectCholesterol effluxen_HK
dc.subjectEndothelial lipaseen_HK
dc.subjectReverse cholesterol transporten_HK
dc.titleEndothelial lipase and reverse cholesterol transport in type 2 diabetes mellitusen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=2040-1116&volume=1&issue=3&spage=111&epage=116&date=2010&atitle=Endothelial+lipase+and+reverse+cholesterol+transport+in+type+2+diabetes+mellitus-
dc.identifier.emailTan, KCB:kcbtan@hku.hken_HK
dc.identifier.authorityTan, KCB=rp00402en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.2040-1124.2010.00016.xen_HK
dc.identifier.scopuseid_2-s2.0-79953752962en_HK
dc.identifier.hkuros174658en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79953752962&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume1en_HK
dc.identifier.issue3en_HK
dc.identifier.spage111en_HK
dc.identifier.epage116en_HK
dc.identifier.isiWOS:000289906300006-
dc.publisher.placeAustraliaen_HK
dc.identifier.scopusauthoridShiu, SWM=7005550652en_HK
dc.identifier.scopusauthoridZhou, H=37162481500en_HK
dc.identifier.scopusauthoridWong, Y=24073787400en_HK
dc.identifier.scopusauthoridTan, KCB=8082703100en_HK
dc.identifier.issnl2040-1116-

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