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Article: Paraoxonase-2 gene (PON2) G148 variant associated with elevated fasting plasma glucose in noninsulin-dependent diabetes mellitus
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TitleParaoxonase-2 gene (PON2) G148 variant associated with elevated fasting plasma glucose in noninsulin-dependent diabetes mellitus
 
AuthorsHegele, RA1
Connelly, PW1
Scherer, SW4
Hanley, AJG3
Harris, SB2
Tsui, LC4
Zinman, B3
 
Issue Date1997
 
PublisherThe Endocrine Society. The Journal's web site is located at http://jcem.endojournals.org
 
CitationJournal Of Clinical Endocrinology And Metabolism, 1997, v. 82 n. 10, p. 3373-3377 [How to Cite?]
DOI: http://dx.doi.org/10.1210/jc.82.10.3373
 
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.
 
Descriptionlink_to_OA_fulltext
 
ISSN0021-972X
2013 Impact Factor: 6.310
2013 SCImago Journal Rankings: 3.169
 
DOIhttp://dx.doi.org/10.1210/jc.82.10.3373
 
ISI Accession Number IDWOS:A1997YA00200038
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorHegele, RA
 
dc.contributor.authorConnelly, PW
 
dc.contributor.authorScherer, SW
 
dc.contributor.authorHanley, AJG
 
dc.contributor.authorHarris, SB
 
dc.contributor.authorTsui, LC
 
dc.contributor.authorZinman, B
 
dc.date.accessioned2011-06-07T02:10:48Z
 
dc.date.available2011-06-07T02:10:48Z
 
dc.date.issued1997
 
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.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.descriptionlink_to_OA_fulltext
 
dc.identifier.citationJournal Of Clinical Endocrinology And Metabolism, 1997, v. 82 n. 10, p. 3373-3377 [How to Cite?]
DOI: http://dx.doi.org/10.1210/jc.82.10.3373
 
dc.identifier.doihttp://dx.doi.org/10.1210/jc.82.10.3373
 
dc.identifier.epage3377
 
dc.identifier.isiWOS:A1997YA00200038
 
dc.identifier.issn0021-972X
2013 Impact Factor: 6.310
2013 SCImago Journal Rankings: 3.169
 
dc.identifier.issue10
 
dc.identifier.openurl
 
dc.identifier.pmid9329371
 
dc.identifier.scopuseid_2-s2.0-0030983832
 
dc.identifier.spage3373
 
dc.identifier.urihttp://hdl.handle.net/10722/133894
 
dc.identifier.volume82
 
dc.languageeng
 
dc.publisherThe Endocrine Society. The Journal's web site is located at http://jcem.endojournals.org
 
dc.publisher.placeUnited States
 
dc.relation.ispartofJournal of Clinical Endocrinology and Metabolism
 
dc.relation.referencesReferences in Scopus
 
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 mellitus
 
dc.typeArticle
 
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Author Affiliations
  1. Saint Michael's Hospital University of Toronto
  2. Western University
  3. University of Toronto
  4. Hospital for Sick Children University of Toronto