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A Variant Upstream of the CDH13 Adiponectin Receptor Gene and Metabolic Syndrome in Swedes.

Fava, Cristiano LU ; Danese, Elisa; Montagnana, Martina LU ; Sjögren, Marketa LU ; Almgren, Peter LU ; Guidi, Gian Cesare; Hedblad, Bo LU ; Engström, Gunnar LU ; Lechi, Alessandro and Minuz, Pietro, et al. (2011) In American Journal of Cardiology 108. p.1432-1437
Abstract
Metabolic syndrome (MetS) constitutes a worldwide epidemic burst accounting for billions of cardiovascular disease events and deaths. The genetic basis of MetS is largely unknown. The rs11646213 T → A polymorphism maps at 16q23.3 upstream of the CDH13 gene codifying for cadherin-13 (also known as T-cadherin or H-cadherin), which is considered a vascular adiponectin receptor. This and other single-nucleotide polymorphisms have been associated with hypertension and adiponectin level in separate studies. The aim of the present study was to evaluate the effect of the CDH13 rs11646213 T → A polymorphism on individual components of MetS and on MetS. The polymorphism was genotyped in the cardiovascular cohort of the Malmö Diet and Cancer Study (n... (More)
Metabolic syndrome (MetS) constitutes a worldwide epidemic burst accounting for billions of cardiovascular disease events and deaths. The genetic basis of MetS is largely unknown. The rs11646213 T → A polymorphism maps at 16q23.3 upstream of the CDH13 gene codifying for cadherin-13 (also known as T-cadherin or H-cadherin), which is considered a vascular adiponectin receptor. This and other single-nucleotide polymorphisms have been associated with hypertension and adiponectin level in separate studies. The aim of the present study was to evaluate the effect of the CDH13 rs11646213 T → A polymorphism on individual components of MetS and on MetS. The polymorphism was genotyped in the cardiovascular cohort of the Malmö Diet and Cancer Study (n = 4,942) and successively in the Malmö Preventive Project (n = 17,675) cohort at baseline and after an average of 23 years of follow-up (reinvestigation). Four different definitions of MetS were applied to these cohorts. In the cardiovascular arm, CDH13 rs11646213 AA homozygotic women showed a trend toward higher triglycerides and lower high-density lipoprotein cholesterol and presented a higher MetS score (composite sum of MetS phenotypes). MetS (Adult Treatment Panel III definition) was more prevalent in AA homozygotic women compared to T-carriers, a result confirmed in the Malmö Preventive Project cohort at baseline and at reinvestigation with an increased risk from 19% to 45% in AA homozygotic women. In conclusion, the CDH13 rs11646213 T > A polymorphism was consistently associated with MetS in Swedish women recruited in 2 large cohorts. In light of the role of cadherin-13 as a vascular receptor for adiponectin, our study supports the genetic basis for the role of adiponectin in MetS pathogenesis. (Less)
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American Journal of Cardiology
volume
108
pages
1432 - 1437
publisher
Excerpta Medica
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  • wos:000297435100010
  • pmid:21872196
  • scopus:80255132037
ISSN
1879-1913
DOI
10.1016/j.amjcard.2011.06.068
language
English
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yes
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69a9b916-d575-44c9-96bf-00e82c57ed8b (old id 2150609)
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http://www.ncbi.nlm.nih.gov/pubmed/21872196?dopt=Abstract
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2011-09-04 12:52:49
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2017-09-03 04:47:20
@article{69a9b916-d575-44c9-96bf-00e82c57ed8b,
  abstract     = {Metabolic syndrome (MetS) constitutes a worldwide epidemic burst accounting for billions of cardiovascular disease events and deaths. The genetic basis of MetS is largely unknown. The rs11646213 T → A polymorphism maps at 16q23.3 upstream of the CDH13 gene codifying for cadherin-13 (also known as T-cadherin or H-cadherin), which is considered a vascular adiponectin receptor. This and other single-nucleotide polymorphisms have been associated with hypertension and adiponectin level in separate studies. The aim of the present study was to evaluate the effect of the CDH13 rs11646213 T → A polymorphism on individual components of MetS and on MetS. The polymorphism was genotyped in the cardiovascular cohort of the Malmö Diet and Cancer Study (n = 4,942) and successively in the Malmö Preventive Project (n = 17,675) cohort at baseline and after an average of 23 years of follow-up (reinvestigation). Four different definitions of MetS were applied to these cohorts. In the cardiovascular arm, CDH13 rs11646213 AA homozygotic women showed a trend toward higher triglycerides and lower high-density lipoprotein cholesterol and presented a higher MetS score (composite sum of MetS phenotypes). MetS (Adult Treatment Panel III definition) was more prevalent in AA homozygotic women compared to T-carriers, a result confirmed in the Malmö Preventive Project cohort at baseline and at reinvestigation with an increased risk from 19% to 45% in AA homozygotic women. In conclusion, the CDH13 rs11646213 T > A polymorphism was consistently associated with MetS in Swedish women recruited in 2 large cohorts. In light of the role of cadherin-13 as a vascular receptor for adiponectin, our study supports the genetic basis for the role of adiponectin in MetS pathogenesis.},
  author       = {Fava, Cristiano and Danese, Elisa and Montagnana, Martina and Sjögren, Marketa and Almgren, Peter and Guidi, Gian Cesare and Hedblad, Bo and Engström, Gunnar and Lechi, Alessandro and Minuz, Pietro and Melander, Olle},
  issn         = {1879-1913},
  language     = {eng},
  pages        = {1432--1437},
  publisher    = {Excerpta Medica},
  series       = {American Journal of Cardiology},
  title        = {A Variant Upstream of the CDH13 Adiponectin Receptor Gene and Metabolic Syndrome in Swedes.},
  url          = {http://dx.doi.org/10.1016/j.amjcard.2011.06.068},
  volume       = {108},
  year         = {2011},
}