The lactase persistence genotype is a protective factor for the metabolic syndrome

Detalhes bibliográficos
Autor(a) principal: Friedrich, Denise Barbosa de Castro
Data de Publicação: 2014
Outros Autores: Andrade, Fabiana Michelsen de, Fiegenbaum, Marilu, Almeida, Silvana de, Mattevi, Vanessa Sune, Callegari-Jacques, Sidia Maria, Hutz, Mara Helena
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UFRGS
Texto Completo: http://hdl.handle.net/10183/118590
Resumo: The Metabolic Syndrome (MetS) is defined as a pattern of metabolic disturbances, which include central obesity, insulin resistance and hyperglycemia, dyslipidemia, and hypertension. Milk has been promoted as a healthy beverage that can improve the management of MetS. Most human adults, however, down-regulate the production of intestinal lactase after weaning. Lactase encoded by the LCT gene is necessary for lactose digestion. The -13910C > T SNP (rs4988235) is responsible for the lactase persistence phenotype in European populations. We herein investigated whether the lactase persistence genotype is also associated with the MetS in subjects from a Brazilian population of European descent. This study consisted of 334 individuals (average age of 41 years) genotyped by PCR-based methods for the -13910C > T SNP. Clinical data were assessed and the genotypes were tested for their independent contribution to the MetS using chi-square tests and multiple logistic regression analysis. Univariate analyses showed that hypertension and MetS prevalence were higher in individuals with the lactase non-persistence genotype than in lactase persistence subjects. Furthermore, lactase persistence was associated with a lower risk for MetS (OR = 0.467; 95% CI 0.264-0.824; p = 0.009). These results suggest that LCT genotypes can be a valuable tool for the management of MetS treatment.
id UFRGS-2_dda0c5d31b5bfa81ae8cb3096cf28002
oai_identifier_str oai:www.lume.ufrgs.br:10183/118590
network_acronym_str UFRGS-2
network_name_str Repositório Institucional da UFRGS
repository_id_str
spelling Friedrich, Denise Barbosa de CastroAndrade, Fabiana Michelsen deFiegenbaum, MariluAlmeida, Silvana deMattevi, Vanessa SuneCallegari-Jacques, Sidia MariaHutz, Mara Helena2015-07-07T02:01:26Z20141415-4757http://hdl.handle.net/10183/118590000952279The Metabolic Syndrome (MetS) is defined as a pattern of metabolic disturbances, which include central obesity, insulin resistance and hyperglycemia, dyslipidemia, and hypertension. Milk has been promoted as a healthy beverage that can improve the management of MetS. Most human adults, however, down-regulate the production of intestinal lactase after weaning. Lactase encoded by the LCT gene is necessary for lactose digestion. The -13910C > T SNP (rs4988235) is responsible for the lactase persistence phenotype in European populations. We herein investigated whether the lactase persistence genotype is also associated with the MetS in subjects from a Brazilian population of European descent. This study consisted of 334 individuals (average age of 41 years) genotyped by PCR-based methods for the -13910C > T SNP. Clinical data were assessed and the genotypes were tested for their independent contribution to the MetS using chi-square tests and multiple logistic regression analysis. Univariate analyses showed that hypertension and MetS prevalence were higher in individuals with the lactase non-persistence genotype than in lactase persistence subjects. Furthermore, lactase persistence was associated with a lower risk for MetS (OR = 0.467; 95% CI 0.264-0.824; p = 0.009). These results suggest that LCT genotypes can be a valuable tool for the management of MetS treatment.application/pdfengGenetics and molecular biology. Ribeirão Preto. Vol. 37, no. 4 (2014), p. 611-615Estatística aplicadaMetabolic syndromeLactase persistenceHypolactasiaLactoseThe lactase persistence genotype is a protective factor for the metabolic syndromeinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/otherinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSORIGINAL000952279.pdf000952279.pdfTexto completo (inglês)application/pdf450501http://www.lume.ufrgs.br/bitstream/10183/118590/1/000952279.pdfa77307fa33248fa7ba56523eec24f397MD51TEXT000952279.pdf.txt000952279.pdf.txtExtracted Texttext/plain22931http://www.lume.ufrgs.br/bitstream/10183/118590/2/000952279.pdf.txt56916f893d2a7f6fe93b53ac97ed2bb1MD5210183/1185902018-06-22 02:29:02.653551oai:www.lume.ufrgs.br:10183/118590Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2018-06-22T05:29:02Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false
dc.title.pt_BR.fl_str_mv The lactase persistence genotype is a protective factor for the metabolic syndrome
title The lactase persistence genotype is a protective factor for the metabolic syndrome
spellingShingle The lactase persistence genotype is a protective factor for the metabolic syndrome
Friedrich, Denise Barbosa de Castro
Estatística aplicada
Metabolic syndrome
Lactase persistence
Hypolactasia
Lactose
title_short The lactase persistence genotype is a protective factor for the metabolic syndrome
title_full The lactase persistence genotype is a protective factor for the metabolic syndrome
title_fullStr The lactase persistence genotype is a protective factor for the metabolic syndrome
title_full_unstemmed The lactase persistence genotype is a protective factor for the metabolic syndrome
title_sort The lactase persistence genotype is a protective factor for the metabolic syndrome
author Friedrich, Denise Barbosa de Castro
author_facet Friedrich, Denise Barbosa de Castro
Andrade, Fabiana Michelsen de
Fiegenbaum, Marilu
Almeida, Silvana de
Mattevi, Vanessa Sune
Callegari-Jacques, Sidia Maria
Hutz, Mara Helena
author_role author
author2 Andrade, Fabiana Michelsen de
Fiegenbaum, Marilu
Almeida, Silvana de
Mattevi, Vanessa Sune
Callegari-Jacques, Sidia Maria
Hutz, Mara Helena
author2_role author
author
author
author
author
author
dc.contributor.author.fl_str_mv Friedrich, Denise Barbosa de Castro
Andrade, Fabiana Michelsen de
Fiegenbaum, Marilu
Almeida, Silvana de
Mattevi, Vanessa Sune
Callegari-Jacques, Sidia Maria
Hutz, Mara Helena
dc.subject.por.fl_str_mv Estatística aplicada
topic Estatística aplicada
Metabolic syndrome
Lactase persistence
Hypolactasia
Lactose
dc.subject.eng.fl_str_mv Metabolic syndrome
Lactase persistence
Hypolactasia
Lactose
description The Metabolic Syndrome (MetS) is defined as a pattern of metabolic disturbances, which include central obesity, insulin resistance and hyperglycemia, dyslipidemia, and hypertension. Milk has been promoted as a healthy beverage that can improve the management of MetS. Most human adults, however, down-regulate the production of intestinal lactase after weaning. Lactase encoded by the LCT gene is necessary for lactose digestion. The -13910C > T SNP (rs4988235) is responsible for the lactase persistence phenotype in European populations. We herein investigated whether the lactase persistence genotype is also associated with the MetS in subjects from a Brazilian population of European descent. This study consisted of 334 individuals (average age of 41 years) genotyped by PCR-based methods for the -13910C > T SNP. Clinical data were assessed and the genotypes were tested for their independent contribution to the MetS using chi-square tests and multiple logistic regression analysis. Univariate analyses showed that hypertension and MetS prevalence were higher in individuals with the lactase non-persistence genotype than in lactase persistence subjects. Furthermore, lactase persistence was associated with a lower risk for MetS (OR = 0.467; 95% CI 0.264-0.824; p = 0.009). These results suggest that LCT genotypes can be a valuable tool for the management of MetS treatment.
publishDate 2014
dc.date.issued.fl_str_mv 2014
dc.date.accessioned.fl_str_mv 2015-07-07T02:01:26Z
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/other
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://hdl.handle.net/10183/118590
dc.identifier.issn.pt_BR.fl_str_mv 1415-4757
dc.identifier.nrb.pt_BR.fl_str_mv 000952279
identifier_str_mv 1415-4757
000952279
url http://hdl.handle.net/10183/118590
dc.language.iso.fl_str_mv eng
language eng
dc.relation.ispartof.pt_BR.fl_str_mv Genetics and molecular biology. Ribeirão Preto. Vol. 37, no. 4 (2014), p. 611-615
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:Repositório Institucional da UFRGS
instname:Universidade Federal do Rio Grande do Sul (UFRGS)
instacron:UFRGS
instname_str Universidade Federal do Rio Grande do Sul (UFRGS)
instacron_str UFRGS
institution UFRGS
reponame_str Repositório Institucional da UFRGS
collection Repositório Institucional da UFRGS
bitstream.url.fl_str_mv http://www.lume.ufrgs.br/bitstream/10183/118590/1/000952279.pdf
http://www.lume.ufrgs.br/bitstream/10183/118590/2/000952279.pdf.txt
bitstream.checksum.fl_str_mv a77307fa33248fa7ba56523eec24f397
56916f893d2a7f6fe93b53ac97ed2bb1
bitstream.checksumAlgorithm.fl_str_mv MD5
MD5
repository.name.fl_str_mv Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)
repository.mail.fl_str_mv
_version_ 1815447587217473536