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Article: A genetic variant in the gene encoding adrenomedullin predicts the development of dysglycemia over 6.4 years in Chinese

TitleA genetic variant in the gene encoding adrenomedullin predicts the development of dysglycemia over 6.4 years in Chinese
Authors
KeywordsAdrenomedullin
Dysglycemia
Single nucleotide polymorphism
Issue Date2011
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/cca
Citation
Clinica Chimica Acta, 2011, v. 412 n. 3-4, p. 353-357 How to Cite?
AbstractBackground: Adrenomedullin, a vasodilatory peptide, facilitates the differentiation of pre-adipocytes, and affects lipolysis and glucose uptake. We investigated the association of common single nucleotide polymorphisms (SNPs) in the gene encoding adrenomedullin (ADM) with dysglycemia in the Hong Kong Chinese population. Methods: Four SNPs were genotyped in 1391 subjects without dysglycemia at baseline from the Hong Kong Cardiovascular Risk Factor Prevalence Study-2, which had a median follow-up time of 6.4. years. Dysglycemia included impaired fasting glucose, impaired glucose tolerance, and diabetes according to the WHO 1998 criteria. At follow-up, 382 subjects had developed dysglycemia. Results: In stepwise logistic regression, the SNP rs11042725 was a significant independent predictor of the development of dysglycemia (OR=1.31, P=0.012), together with baseline age (P< 0.001), plasma triglycerides (P< 0.001), body mass index (P=0.004), 2-h glucose after oral glucose tolerance test (P< 0.001), homeostasis model assessment of insulin resistance index (P=0.045), and follow-up duration (P=0.009). The association was more significant in women (P=0.002) and in subjects without regular exercise (P=0.001). Conclusions: Our study suggests a potential role of genetic variants in the ADM gene in the development of dysglycemia in our local Chinese population. © 2010 Elsevier B.V.
Persistent Identifierhttp://hdl.handle.net/10722/129273
ISSN
2014 Impact Factor: 2.824
2013 SCImago Journal Rankings: 1.039
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grant CouncilHKU7229/01 M
HKU7626/07 M
Sun Chieh Yeh Heart Foundation
Funding Information:

This study was funded by Hong Kong Research Grant Council grants (HKU7229/01 M and HKU7626/07 M), and the Sun Chieh Yeh Heart Foundation.

References

 

DC FieldValueLanguage
dc.contributor.authorOng, KLen_HK
dc.contributor.authorTso, AWKen_HK
dc.contributor.authorLeung, RYHen_HK
dc.contributor.authorCherny, SSen_HK
dc.contributor.authorSham, PCen_HK
dc.contributor.authorLam, THen_HK
dc.contributor.authorCheung, BMYen_HK
dc.contributor.authorLam, KSLen_HK
dc.date.accessioned2010-12-23T08:34:34Z-
dc.date.available2010-12-23T08:34:34Z-
dc.date.issued2011en_HK
dc.identifier.citationClinica Chimica Acta, 2011, v. 412 n. 3-4, p. 353-357en_HK
dc.identifier.issn0009-8981en_HK
dc.identifier.urihttp://hdl.handle.net/10722/129273-
dc.description.abstractBackground: Adrenomedullin, a vasodilatory peptide, facilitates the differentiation of pre-adipocytes, and affects lipolysis and glucose uptake. We investigated the association of common single nucleotide polymorphisms (SNPs) in the gene encoding adrenomedullin (ADM) with dysglycemia in the Hong Kong Chinese population. Methods: Four SNPs were genotyped in 1391 subjects without dysglycemia at baseline from the Hong Kong Cardiovascular Risk Factor Prevalence Study-2, which had a median follow-up time of 6.4. years. Dysglycemia included impaired fasting glucose, impaired glucose tolerance, and diabetes according to the WHO 1998 criteria. At follow-up, 382 subjects had developed dysglycemia. Results: In stepwise logistic regression, the SNP rs11042725 was a significant independent predictor of the development of dysglycemia (OR=1.31, P=0.012), together with baseline age (P< 0.001), plasma triglycerides (P< 0.001), body mass index (P=0.004), 2-h glucose after oral glucose tolerance test (P< 0.001), homeostasis model assessment of insulin resistance index (P=0.045), and follow-up duration (P=0.009). The association was more significant in women (P=0.002) and in subjects without regular exercise (P=0.001). Conclusions: Our study suggests a potential role of genetic variants in the ADM gene in the development of dysglycemia in our local Chinese population. © 2010 Elsevier B.V.en_HK
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ccaen_HK
dc.relation.ispartofClinica Chimica Actaen_HK
dc.rightsAppropriate Bibliographic Citation:Authors posting Accepted Author Manuscript online should later add a citation for the Published Journal Article indicating that the Article was subsequently published, and may mention the journal title provided that they add the following text at the beginning of the document: “NOTICE: this is the author’s version of a work that was accepted for publication in <Journal title>. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in PUBLICATION, [VOL#, ISSUE#, (DATE)] DOI#”-
dc.subjectAdrenomedullinen_HK
dc.subjectDysglycemiaen_HK
dc.subjectSingle nucleotide polymorphismen_HK
dc.titleA genetic variant in the gene encoding adrenomedullin predicts the development of dysglycemia over 6.4 years in Chineseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0009-8981&volume=412&issue=3-4&spage=353&epage=357&date=2010&atitle=A+genetic+variant+in+the+gene+encoding+adrenomedullin+predicts+the+development+of+dysglycemia+over+6.4+years+in+Chinese-
dc.identifier.emailTso, AWK: awk.tso@gmail.comen_HK
dc.identifier.emailCherny, SS: cherny@hku.hken_HK
dc.identifier.emailSham, PC: pcsham@hku.hken_HK
dc.identifier.emailLam, TH: hrmrlth@hkucc.hku.hken_HK
dc.identifier.emailCheung, BMY: mycheung@hku.hken_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.authorityTso, AWK=rp00535en_HK
dc.identifier.authorityCherny, SS=rp00232en_HK
dc.identifier.authoritySham, PC=rp00459en_HK
dc.identifier.authorityLam, TH=rp00326en_HK
dc.identifier.authorityCheung, BMY=rp01321en_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.cca.2010.11.007en_HK
dc.identifier.pmid21075100en_HK
dc.identifier.scopuseid_2-s2.0-78650237267en_HK
dc.identifier.hkuros183469en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78650237267&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume412en_HK
dc.identifier.issue3-4en_HK
dc.identifier.spage353en_HK
dc.identifier.epage357en_HK
dc.identifier.isiWOS:000287115400024-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridOng, KL=8340854000en_HK
dc.identifier.scopusauthoridTso, AWK=6701371436en_HK
dc.identifier.scopusauthoridLeung, RYH=7101876102en_HK
dc.identifier.scopusauthoridCherny, SS=7004670001en_HK
dc.identifier.scopusauthoridSham, PC=34573429300en_HK
dc.identifier.scopusauthoridLam, TH=7202522876en_HK
dc.identifier.scopusauthoridCheung, BMY=7103294806en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK
dc.identifier.citeulike8266126-

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