File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Effects of testosterone replacement on HDL subfractions and apolipoprotein A-I containing lipoproteins

TitleEffects of testosterone replacement on HDL subfractions and apolipoprotein A-I containing lipoproteins
Authors
Issue Date1998
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0300-0664
Citation
Clinical Endocrinology, 1998, v. 48 n. 2, p. 187-194 How to Cite?
AbstractOBJECTIVES: Gonadal steroids are important regulators of lipoprotein metabolism. The aims of this study were to determine the effects of a minimum effective dose of testosterone replacement on high density lipoprotein (HDL) subfractions and apolipoprotein (apo) A-I containing particles (lipoprotein (Lp)A-I) and LpA-I:A-II) in hypogonadal men with primary testicular failure and to investigate the underlying mechanisms of these changes. MEASUREMENTS: Eleven Chinese hypogonadal men were started on testosterone enanthate 250 mg intramuscularly at 4-weekly intervals. HDL was subfractionated by density gradient ultracentrifugation and LpA-I was analysed by electro- immunodiffusion after 3, 6 and 12 weeks of treatment. Plasma cholesteryl ester transfer protein (CETP) activity and lipolytic enzymes activities in post-heparin plasma were measured to determine the mechanisms underlying testosterone-induced changes in HDL. RESULTS: The dosage of testosterone enanthate used in the present study resulted in suboptimal trough testosterone levels. No changes were seen in plasma total cholesterol, triglyceride, low density lipoprotein cholesterol (LDL-C,) apo B and apo(a) after 12 weeks. There was a drop in HDL3-C compared to baseline (0.82 ± 0.17 mmol/1 vs. 0.93 ± 0.13, P< 0.01) whereas a small but significant increase was seen in HDL2-C (0.21 ± 0.13 mmol/vs. 0.11 ± 0.09, P<0.05). Plasma apo A-I decreased after treatment (1.34 ± 0.25 g/l vs. 1.50 ± 0.29, P<0.01), due to a reduction in LpA-I:A-II particles (0.86 ± 0.18 g/l vs. 0.99 ± 0.24, P<0.01). No changes were observed in the levels of LpA-I particles. No significant changes were seen in plasma CETP and lipoprotein lipase activities after testosterone replacement but there was a transient increase in hepatic lipase (HL) activity at weeks 3 and 6. The decrease in HDL correlated with the increase in HL activity (r= 0.62, P< 0.05). CONCLUSIONS: Testosterone replacement in the form of parenteral testosterone ester given 4-weekly, although unphysiological, was not associated with unfavourable changes in lipid profiles. The reduction in HDL was mainly in HDL3-C and in LpA-I:A-II particles and not in the more anti-atherogenic HDL2 and LpA-I particles. The changes in HDL subclasses were mainly mediated through the effect of testosterone on hepatic lipase activity.
Persistent Identifierhttp://hdl.handle.net/10722/162239
ISSN
2023 Impact Factor: 3.0
2023 SCImago Journal Rankings: 0.978
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTan, KCBen_HK
dc.contributor.authorShiu, SWMen_HK
dc.contributor.authorPang, RWCen_HK
dc.contributor.authorKung, AWCen_HK
dc.date.accessioned2012-09-05T05:18:20Z-
dc.date.available2012-09-05T05:18:20Z-
dc.date.issued1998en_HK
dc.identifier.citationClinical Endocrinology, 1998, v. 48 n. 2, p. 187-194en_HK
dc.identifier.issn0300-0664en_HK
dc.identifier.urihttp://hdl.handle.net/10722/162239-
dc.description.abstractOBJECTIVES: Gonadal steroids are important regulators of lipoprotein metabolism. The aims of this study were to determine the effects of a minimum effective dose of testosterone replacement on high density lipoprotein (HDL) subfractions and apolipoprotein (apo) A-I containing particles (lipoprotein (Lp)A-I) and LpA-I:A-II) in hypogonadal men with primary testicular failure and to investigate the underlying mechanisms of these changes. MEASUREMENTS: Eleven Chinese hypogonadal men were started on testosterone enanthate 250 mg intramuscularly at 4-weekly intervals. HDL was subfractionated by density gradient ultracentrifugation and LpA-I was analysed by electro- immunodiffusion after 3, 6 and 12 weeks of treatment. Plasma cholesteryl ester transfer protein (CETP) activity and lipolytic enzymes activities in post-heparin plasma were measured to determine the mechanisms underlying testosterone-induced changes in HDL. RESULTS: The dosage of testosterone enanthate used in the present study resulted in suboptimal trough testosterone levels. No changes were seen in plasma total cholesterol, triglyceride, low density lipoprotein cholesterol (LDL-C,) apo B and apo(a) after 12 weeks. There was a drop in HDL3-C compared to baseline (0.82 ± 0.17 mmol/1 vs. 0.93 ± 0.13, P< 0.01) whereas a small but significant increase was seen in HDL2-C (0.21 ± 0.13 mmol/vs. 0.11 ± 0.09, P<0.05). Plasma apo A-I decreased after treatment (1.34 ± 0.25 g/l vs. 1.50 ± 0.29, P<0.01), due to a reduction in LpA-I:A-II particles (0.86 ± 0.18 g/l vs. 0.99 ± 0.24, P<0.01). No changes were observed in the levels of LpA-I particles. No significant changes were seen in plasma CETP and lipoprotein lipase activities after testosterone replacement but there was a transient increase in hepatic lipase (HL) activity at weeks 3 and 6. The decrease in HDL correlated with the increase in HL activity (r= 0.62, P< 0.05). CONCLUSIONS: Testosterone replacement in the form of parenteral testosterone ester given 4-weekly, although unphysiological, was not associated with unfavourable changes in lipid profiles. The reduction in HDL was mainly in HDL3-C and in LpA-I:A-II particles and not in the more anti-atherogenic HDL2 and LpA-I particles. The changes in HDL subclasses were mainly mediated through the effect of testosterone on hepatic lipase activity.en_HK
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0300-0664en_HK
dc.relation.ispartofClinical Endocrinologyen_HK
dc.rightsClinical Endocrinology. Copyright © Blackwell Publishing Ltd.-
dc.subject.meshAdulten_US
dc.subject.meshApolipoprotein A-I - Metabolismen_US
dc.subject.meshCarrier Proteins - Blooden_US
dc.subject.meshCholesterol - Blooden_US
dc.subject.meshCholesterol Ester Transfer Proteinsen_US
dc.subject.meshEstradiol - Blooden_US
dc.subject.meshFollicle Stimulating Hormone - Blooden_US
dc.subject.meshGlycoproteinsen_US
dc.subject.meshHumansen_US
dc.subject.meshHypogonadism - Blood - Drug Therapyen_US
dc.subject.meshLipase - Metabolismen_US
dc.subject.meshLipoproteins, Hdl - Metabolismen_US
dc.subject.meshLiver - Enzymologyen_US
dc.subject.meshLuteinizing Hormone - Blooden_US
dc.subject.meshMaleen_US
dc.subject.meshTestosterone - Blood - Therapeutic Useen_US
dc.subject.meshTriglycerides - Blooden_US
dc.titleEffects of testosterone replacement on HDL subfractions and apolipoprotein A-I containing lipoproteinsen_HK
dc.typeArticleen_HK
dc.identifier.emailTan, KCB: kcbtan@hku.hken_HK
dc.identifier.emailPang, RWC: robertap@hkucc.hku.hken_HK
dc.identifier.emailKung, AWC: awckung@hku.hken_HK
dc.identifier.authorityTan, KCB=rp00402en_HK
dc.identifier.authorityPang, RWC=rp00274en_HK
dc.identifier.authorityKung, AWC=rp00368en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1046/j.1365-2265.1998.00372.xen_HK
dc.identifier.pmid9579231-
dc.identifier.scopuseid_2-s2.0-0031887049en_HK
dc.identifier.hkuros38403-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031887049&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume48en_HK
dc.identifier.issue2en_HK
dc.identifier.spage187en_HK
dc.identifier.epage194en_HK
dc.identifier.isiWOS:000072120800011-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridTan, KCB=8082703100en_HK
dc.identifier.scopusauthoridShiu, SWM=7005550652en_HK
dc.identifier.scopusauthoridPang, RWC=7004376659en_HK
dc.identifier.scopusauthoridKung, AWC=7102322339en_HK
dc.identifier.issnl0300-0664-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats