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Article: Roles of hepatic lipase and cholesteryl ester transfer protein in determining low density lipoprotein subfraction distribution in Chinese patients with non-insulin-dependent diabetes mellitus

TitleRoles of hepatic lipase and cholesteryl ester transfer protein in determining low density lipoprotein subfraction distribution in Chinese patients with non-insulin-dependent diabetes mellitus
Authors
Issue Date1999
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis
Citation
Atherosclerosis, 1999, v. 145 n. 2, p. 273-278 How to Cite?
AbstractPatients with non-insulin-dependent diabetes mellitus (NIDDM) are known to have abnormalities in their low density lipoprotein (LDL) subclass pattern with a preponderance of small dense LDL. The present study was performed to define the roles of lipolytic enzymes (hepatic and lipoprotein lipase) and cholesteryl ester transfer protein (CETP) in determining the distribution of LDL subfractions in these patients. LDL subfractions were measured by density gradient ultracentrifugation in 137 patients with NIDDM (75 male, 62 female) and 140 matched controls (80 male, 60 female). The male diabetic patients had a lower concentration of LDL-I (P<0.01) and a higher concentration of LDL-III than the controls (P<0.01). In the female diabetic patients, both LDL-I (P<0.001) and LDL-II concentrations (P<0.05) were significantly lower than the controls whereas LDL-III was increased (P<0.001). Hepatic lipase (HL) was significantly increased in both the male and female diabetic patients (P<0.01, P<0.05, respectively) compared to their controls. No significant changes were seen in plasma lipoprotein lipase (LPL) and CETP activity. On multivariate analysis, plasma triglyceride (TG), CETP and HL accounted for 10, 5 and 3% of the variability in LDL-III, respectively, in the diabetic patients (adjusted R2=0.18, P=0.0003). Our findings would support the hypothesis that plasma triglyceride influences LDL particles through a cycle of lipid exchange via the action of CETP. LDL become enriched in triglyceride and are then acted on by HL to produce a population of small dense lipid-poor LDL. Copyright (C) 1999 Elsevier Science Ireland Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/162295
ISSN
2015 Impact Factor: 3.942
2015 SCImago Journal Rankings: 1.819
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTan, KCBen_US
dc.contributor.authorShiu, SWMen_US
dc.contributor.authorChu, BYMen_US
dc.date.accessioned2012-09-05T05:18:43Z-
dc.date.available2012-09-05T05:18:43Z-
dc.date.issued1999en_US
dc.identifier.citationAtherosclerosis, 1999, v. 145 n. 2, p. 273-278en_US
dc.identifier.issn0021-9150en_US
dc.identifier.urihttp://hdl.handle.net/10722/162295-
dc.description.abstractPatients with non-insulin-dependent diabetes mellitus (NIDDM) are known to have abnormalities in their low density lipoprotein (LDL) subclass pattern with a preponderance of small dense LDL. The present study was performed to define the roles of lipolytic enzymes (hepatic and lipoprotein lipase) and cholesteryl ester transfer protein (CETP) in determining the distribution of LDL subfractions in these patients. LDL subfractions were measured by density gradient ultracentrifugation in 137 patients with NIDDM (75 male, 62 female) and 140 matched controls (80 male, 60 female). The male diabetic patients had a lower concentration of LDL-I (P<0.01) and a higher concentration of LDL-III than the controls (P<0.01). In the female diabetic patients, both LDL-I (P<0.001) and LDL-II concentrations (P<0.05) were significantly lower than the controls whereas LDL-III was increased (P<0.001). Hepatic lipase (HL) was significantly increased in both the male and female diabetic patients (P<0.01, P<0.05, respectively) compared to their controls. No significant changes were seen in plasma lipoprotein lipase (LPL) and CETP activity. On multivariate analysis, plasma triglyceride (TG), CETP and HL accounted for 10, 5 and 3% of the variability in LDL-III, respectively, in the diabetic patients (adjusted R2=0.18, P=0.0003). Our findings would support the hypothesis that plasma triglyceride influences LDL particles through a cycle of lipid exchange via the action of CETP. LDL become enriched in triglyceride and are then acted on by HL to produce a population of small dense lipid-poor LDL. Copyright (C) 1999 Elsevier Science Ireland Ltd.en_US
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosisen_US
dc.relation.ispartofAtherosclerosisen_US
dc.rightsAtherosclerosis. Copyright © Elsevier Ireland Ltd.-
dc.subject.meshAsian Continental Ancestry Groupen_US
dc.subject.meshBiological Markers - Blooden_US
dc.subject.meshCarrier Proteins - Metabolismen_US
dc.subject.meshCholesterol Ester Transfer Proteinsen_US
dc.subject.meshCoronary Artery Disease - Blood - Etiologyen_US
dc.subject.meshDiabetes Mellitus, Type 2 - Blood - Ethnologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGlycoproteinsen_US
dc.subject.meshHemoglobin A, Glycosylated - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshLipoprotein Lipase - Metabolismen_US
dc.subject.meshLipoproteins, Hdl - Blooden_US
dc.subject.meshLipoproteins, Ldl - Blooden_US
dc.subject.meshLiver - Enzymologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshSex Characteristicsen_US
dc.subject.meshTriglycerides - Blooden_US
dc.subject.meshUltracentrifugationen_US
dc.titleRoles of hepatic lipase and cholesteryl ester transfer protein in determining low density lipoprotein subfraction distribution in Chinese patients with non-insulin-dependent diabetes mellitusen_US
dc.typeArticleen_US
dc.identifier.emailTan, KCB:kcbtan@hku.hken_US
dc.identifier.authorityTan, KCB=rp00402en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0021-9150(99)00077-5en_US
dc.identifier.pmid10488953-
dc.identifier.scopuseid_2-s2.0-0032767646en_US
dc.identifier.hkuros51182-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032767646&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume145en_US
dc.identifier.issue2en_US
dc.identifier.spage273en_US
dc.identifier.epage278en_US
dc.identifier.isiWOS:000082324000006-
dc.publisher.placeIrelanden_US
dc.identifier.scopusauthoridTan, KCB=8082703100en_US
dc.identifier.scopusauthoridShiu, SWM=7005550652en_US
dc.identifier.scopusauthoridChu, BYM=7202962716en_US

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