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Article: Paraoxonase-2 gene (PON2) G148 variant associated with elevated fasting plasma glucose in noninsulin-dependent diabetes mellitus

TitleParaoxonase-2 gene (PON2) G148 variant associated with elevated fasting plasma glucose in noninsulin-dependent diabetes mellitus
Authors
Issue Date1997
PublisherThe Endocrine Society. The Journal's web site is located at http://jcem.endojournals.org
Citation
Journal Of Clinical Endocrinology And Metabolism, 1997, v. 82 n. 10, p. 3373-3377 How to Cite?
Abstract
Defining the genetic determinants of NIDDM requires evidence from several complementary approaches, including both linkage and association analyses using both discrete phenotypes and intermediate quantitative traits. We tested for association between common genomic variation in three genes that map to chromosome 7q21-q22 and quantitative traits related to NIDDM in a sample of Oji-Cree. We found that a common genomic variation in codon 148 (alanine or glycine) of the paraoxonase-2 gene (PON2) demonstrated a significant association with a variation in fasting plasma glucose (P < 0.0001). Furthermore, we found a significant association between a variation in fasting plasma glucose and the interaction term comprised of a PON2 codon 148 genetic variation and the presence of noninsulin-dependent diabetes mellitus (NIDDM;P < 0.0001). We then analyzed subjects according to PON2 genotype and NIDDM status. In subjects with NIDDM, the PON2 codon 148 G/G homozygotes had significantly higher mean fasting plasma glucose than subjects with the other two genotypes (P < 0.0001). However, in non-NIDDM subjects, there was no difference in mean fasting plasma glucose among any of the genotypes. There was no association of the PON2 genotype with NIDDM itself, with impaired glucose tolerance, or with other quantitative traits related to NIDDM in this sample. These findings suggest that 1) the PON2 G148 gene variant worsens glycemia in subjects with NIDDM; 2) defining the physiological role of the PON2 gene product would be worthwhile; and 3) genetic factors can modify the severity of clinical phenotypes in subjects with NIDDM.
Descriptionlink_to_OA_fulltext
Persistent Identifierhttp://hdl.handle.net/10722/133894
ISSN
2013 Impact Factor: 6.310
2013 SCImago Journal Rankings: 3.169
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHegele, RAen_HK
dc.contributor.authorConnelly, PWen_HK
dc.contributor.authorScherer, SWen_HK
dc.contributor.authorHanley, AJGen_HK
dc.contributor.authorHarris, SBen_HK
dc.contributor.authorTsui, LCen_HK
dc.contributor.authorZinman, Ben_HK
dc.date.accessioned2011-06-07T02:10:48Z-
dc.date.available2011-06-07T02:10:48Z-
dc.date.issued1997en_HK
dc.identifier.citationJournal Of Clinical Endocrinology And Metabolism, 1997, v. 82 n. 10, p. 3373-3377en_HK
dc.identifier.issn0021-972Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/133894-
dc.descriptionlink_to_OA_fulltext-
dc.description.abstractDefining the genetic determinants of NIDDM requires evidence from several complementary approaches, including both linkage and association analyses using both discrete phenotypes and intermediate quantitative traits. We tested for association between common genomic variation in three genes that map to chromosome 7q21-q22 and quantitative traits related to NIDDM in a sample of Oji-Cree. We found that a common genomic variation in codon 148 (alanine or glycine) of the paraoxonase-2 gene (PON2) demonstrated a significant association with a variation in fasting plasma glucose (P < 0.0001). Furthermore, we found a significant association between a variation in fasting plasma glucose and the interaction term comprised of a PON2 codon 148 genetic variation and the presence of noninsulin-dependent diabetes mellitus (NIDDM;P < 0.0001). We then analyzed subjects according to PON2 genotype and NIDDM status. In subjects with NIDDM, the PON2 codon 148 G/G homozygotes had significantly higher mean fasting plasma glucose than subjects with the other two genotypes (P < 0.0001). However, in non-NIDDM subjects, there was no difference in mean fasting plasma glucose among any of the genotypes. There was no association of the PON2 genotype with NIDDM itself, with impaired glucose tolerance, or with other quantitative traits related to NIDDM in this sample. These findings suggest that 1) the PON2 G148 gene variant worsens glycemia in subjects with NIDDM; 2) defining the physiological role of the PON2 gene product would be worthwhile; and 3) genetic factors can modify the severity of clinical phenotypes in subjects with NIDDM.en_HK
dc.languageeng-
dc.publisherThe Endocrine Society. The Journal's web site is located at http://jcem.endojournals.orgen_HK
dc.relation.ispartofJournal of Clinical Endocrinology and Metabolismen_HK
dc.subject.meshBlood Glucose - analysis-
dc.subject.meshDiabetes Mellitus, Type 2 - blood - genetics-
dc.subject.meshEsterases - genetics-
dc.subject.meshFasting-
dc.subject.meshGenetic Variation-
dc.titleParaoxonase-2 gene (PON2) G148 variant associated with elevated fasting plasma glucose in noninsulin-dependent diabetes mellitusen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-972X&volume=82&issue=10&spage=3373&epage=3377&date=1997&atitle=Paraoxonase-2+gene+(PON2)+G148+variant+associated+with+elevated+fasting+plasma+glucose+in+noninsulin-dependent+diabetes+mellitus-
dc.identifier.emailTsui, LC: tsuilc@hkucc.hku.hken_HK
dc.identifier.authorityTsui, LC=rp00058en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1210/jc.82.10.3373en_HK
dc.identifier.pmid9329371en_HK
dc.identifier.scopuseid_2-s2.0-0030983832en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030983832&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume82en_HK
dc.identifier.issue10en_HK
dc.identifier.spage3373en_HK
dc.identifier.epage3377en_HK
dc.identifier.isiWOS:A1997YA00200038-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHegele, RA=35399481100en_HK
dc.identifier.scopusauthoridConnelly, PW=16738577100en_HK
dc.identifier.scopusauthoridScherer, SW=35374654500en_HK
dc.identifier.scopusauthoridHanley, AJG=7005599486en_HK
dc.identifier.scopusauthoridHarris, SB=35500171900en_HK
dc.identifier.scopusauthoridTsui, LC=7102754167en_HK
dc.identifier.scopusauthoridZinman, B=7102090193en_HK

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