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Article: Adiponectin isoform distribution in women-relationship to female sex steroids and insulin sensitivity

TitleAdiponectin isoform distribution in women-relationship to female sex steroids and insulin sensitivity
Authors
Issue Date2009
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/metabol
Citation
Metabolism: Clinical And Experimental, 2009, v. 58 n. 2, p. 239-245 How to Cite?
AbstractLittle is known about the associations between adiponectin and its oligomeric isoforms with female sex steroids, and the relevance of these relationships to insulin sensitivity in women. In a cross-sectional study of 32 healthy women (12 premenopausal, 10 postmenopausal, and 10 early pregnant), we investigated the correlations of total adiponectin and the high-, medium-, and low-molecular weight oligomers (HMW, MMW, and LMW, respectively) with estrogen, progesterone, adiposity, and insulin resistance. Fat mass and serum concentrations of estradiol, progesterone, insulin, glucose, and total and isoform adiponectin were measured. The homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. Serum concentrations of total and HMW adiponectin were highest in postmenopausal women and lowest in pregnant women. Concentrations of the MMW and LMW isoforms were not significantly different between the 3 groups. Total adiponectin, HMW adiponectin, and MMW adiponectin were negatively associated with estradiol and progesterone; but no associations between the LMW isoform and female sex steroids were observed. Fat mass and HOMA-IR were highest in pregnant women and lowest in premenopausal women. The HOMA-IR was positively associated with fat mass, estradiol, and progesterone, and negatively associated with total, HMW, and MMW adiponectin. Multivariate stepwise regression analysis revealed that fat mass explained 34% of the variance in HOMA-IR and that total and isoform adiponectin contributed an additional 10% to 15%. In the multivariate linear regression analysis, there were significant interactions of estradiol and progesterone with adiponectin or fat mass in the associations with HOMA-IR. In conclusion, there are strong negative associations of serum adiponectin and some of its isoforms with estradiol and progesterone. Female sex steroids are likely to affect insulin sensitivity through modulation of adiponectin and body fat. © 2009 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/163224
ISSN
2021 Impact Factor: 13.934
2020 SCImago Journal Rankings: 2.177
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, KCen_US
dc.contributor.authorXu, Aen_US
dc.contributor.authorCraig, MEen_US
dc.contributor.authorMartin, Aen_US
dc.contributor.authorLam, KSLen_US
dc.contributor.authorO'sullivan, AJen_US
dc.date.accessioned2012-09-05T05:28:55Z-
dc.date.available2012-09-05T05:28:55Z-
dc.date.issued2009en_US
dc.identifier.citationMetabolism: Clinical And Experimental, 2009, v. 58 n. 2, p. 239-245en_US
dc.identifier.issn0026-0495en_US
dc.identifier.urihttp://hdl.handle.net/10722/163224-
dc.description.abstractLittle is known about the associations between adiponectin and its oligomeric isoforms with female sex steroids, and the relevance of these relationships to insulin sensitivity in women. In a cross-sectional study of 32 healthy women (12 premenopausal, 10 postmenopausal, and 10 early pregnant), we investigated the correlations of total adiponectin and the high-, medium-, and low-molecular weight oligomers (HMW, MMW, and LMW, respectively) with estrogen, progesterone, adiposity, and insulin resistance. Fat mass and serum concentrations of estradiol, progesterone, insulin, glucose, and total and isoform adiponectin were measured. The homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. Serum concentrations of total and HMW adiponectin were highest in postmenopausal women and lowest in pregnant women. Concentrations of the MMW and LMW isoforms were not significantly different between the 3 groups. Total adiponectin, HMW adiponectin, and MMW adiponectin were negatively associated with estradiol and progesterone; but no associations between the LMW isoform and female sex steroids were observed. Fat mass and HOMA-IR were highest in pregnant women and lowest in premenopausal women. The HOMA-IR was positively associated with fat mass, estradiol, and progesterone, and negatively associated with total, HMW, and MMW adiponectin. Multivariate stepwise regression analysis revealed that fat mass explained 34% of the variance in HOMA-IR and that total and isoform adiponectin contributed an additional 10% to 15%. In the multivariate linear regression analysis, there were significant interactions of estradiol and progesterone with adiponectin or fat mass in the associations with HOMA-IR. In conclusion, there are strong negative associations of serum adiponectin and some of its isoforms with estradiol and progesterone. Female sex steroids are likely to affect insulin sensitivity through modulation of adiponectin and body fat. © 2009 Elsevier Inc. All rights reserved.en_US
dc.languageengen_US
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/metabolen_US
dc.relation.ispartofMetabolism: Clinical and Experimentalen_US
dc.subject.meshAdiponectin - Blood - Chemistryen_US
dc.subject.meshAdipose Tissue - Metabolismen_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshBlood Glucose - Metabolismen_US
dc.subject.meshCross-Sectional Studiesen_US
dc.subject.meshEstradiol - Blooden_US
dc.subject.meshFemaleen_US
dc.subject.meshHomeostasis - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshInsulin - Blooden_US
dc.subject.meshInsulin Resistance - Physiologyen_US
dc.subject.meshIsomerismen_US
dc.subject.meshLinear Modelsen_US
dc.subject.meshMolecular Weighten_US
dc.subject.meshMultivariate Analysisen_US
dc.subject.meshPregnancyen_US
dc.subject.meshProgesterone - Blooden_US
dc.titleAdiponectin isoform distribution in women-relationship to female sex steroids and insulin sensitivityen_US
dc.typeArticleen_US
dc.identifier.emailXu, A:amxu@hkucc.hku.hken_US
dc.identifier.emailLam, KSL:ksllam@hku.hken_US
dc.identifier.authorityXu, A=rp00485en_US
dc.identifier.authorityLam, KSL=rp00343en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.metabol.2008.09.020en_US
dc.identifier.pmid19154958-
dc.identifier.scopuseid_2-s2.0-58249130623en_US
dc.identifier.hkuros155047-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-58249130623&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume58en_US
dc.identifier.issue2en_US
dc.identifier.spage239en_US
dc.identifier.epage245en_US
dc.identifier.isiWOS:000263044400014-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLeung, KC=36056975100en_US
dc.identifier.scopusauthoridXu, A=7202655409en_US
dc.identifier.scopusauthoridCraig, ME=7103269737en_US
dc.identifier.scopusauthoridMartin, A=8642051200en_US
dc.identifier.scopusauthoridLam, KSL=8082870600en_US
dc.identifier.scopusauthoridO'Sullivan, AJ=7007014483en_US
dc.identifier.citeulike4373459-
dc.identifier.issnl0026-0495-

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