Vitamin D Receptor Gene Polymorphisms, β-cell Function, and Vitamin D Status in Non-obese Mexican Adults.


Journal

Archives of medical research
ISSN: 1873-5487
Titre abrégé: Arch Med Res
Pays: United States
ID NLM: 9312706

Informations de publication

Date de publication:
06 2022
Historique:
received: 21 07 2021
revised: 24 03 2022
accepted: 06 04 2022
pubmed: 3 5 2022
medline: 31 5 2022
entrez: 2 5 2022
Statut: ppublish

Résumé

FokI (rs2228570 T>C) and BsmI (rs1544410 A>G) polymorphisms of the vitamin D receptor (VDR) have been associated to abnormal glucose metabolism and could be inversely associated with β-cell function (BCF) and vitamin D status. There is a lack of information about this topic in the Mexican population. To evaluate the relationship between VDR gene polymorphisms FokI and BsmI with BCF and vitamin D status in a population of non-obese Mexican adults. A sample of 192 participants were enrolled during 2016-2018. Blood samples were collected to determine fasting concentrations of glucose, insulin, and vitamin D. Genomic DNA was isolated from leucocytes and the polymorphic variants of FokI and BsmI were analyzed. The Homeostasis Model Assessment Calculator was used to estimate the BCF (HOMA2-B). FokI polymorphism showed a frequency of 20.1% for homozygous TT carriers and 7.8% for the BsmI GG. The recessive model of FokI (TT genotype) showed a lower mean value of BCF compared to the combination of CC + CT (99.2 vs. 109.6%, p = 0.045). Likewise, significantly lower mean values of HOMA2-B and insulin were observed for BsmI (GG genotype, p = 0.016 and p = 0.039, respectively). After covariates adjustment, only FokI polymorphism remained as an independent predictor of BCF. the TT and GG variants of the FokI and BsmI polymorphisms are related to a decrease in FCB. In the case of FokI, this decrement was independent of insulin sensitivity, vitamin D levels, percentage of body fat, gender, and age.

Sections du résumé

BACKGROUND
FokI (rs2228570 T>C) and BsmI (rs1544410 A>G) polymorphisms of the vitamin D receptor (VDR) have been associated to abnormal glucose metabolism and could be inversely associated with β-cell function (BCF) and vitamin D status. There is a lack of information about this topic in the Mexican population.
AIM OF THE STUDY
To evaluate the relationship between VDR gene polymorphisms FokI and BsmI with BCF and vitamin D status in a population of non-obese Mexican adults.
METHODS
A sample of 192 participants were enrolled during 2016-2018. Blood samples were collected to determine fasting concentrations of glucose, insulin, and vitamin D. Genomic DNA was isolated from leucocytes and the polymorphic variants of FokI and BsmI were analyzed. The Homeostasis Model Assessment Calculator was used to estimate the BCF (HOMA2-B).
RESULTS
FokI polymorphism showed a frequency of 20.1% for homozygous TT carriers and 7.8% for the BsmI GG. The recessive model of FokI (TT genotype) showed a lower mean value of BCF compared to the combination of CC + CT (99.2 vs. 109.6%, p = 0.045). Likewise, significantly lower mean values of HOMA2-B and insulin were observed for BsmI (GG genotype, p = 0.016 and p = 0.039, respectively). After covariates adjustment, only FokI polymorphism remained as an independent predictor of BCF.
CONCLUSIONS
the TT and GG variants of the FokI and BsmI polymorphisms are related to a decrease in FCB. In the case of FokI, this decrement was independent of insulin sensitivity, vitamin D levels, percentage of body fat, gender, and age.

Identifiants

pubmed: 35501225
pii: S0188-4409(22)00044-3
doi: 10.1016/j.arcmed.2022.04.002
pii:
doi:

Substances chimiques

Insulins 0
Receptors, Calcitriol 0
VDR protein, human 0
Vitamin D 1406-16-2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

416-422

Informations de copyright

Copyright © 2022. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Conflict of Interest All authors declare no conflict of interest.

Auteurs

Mónica Ivette Piña-Aguero (MI)

Unidad de Investigación Médica en Nutrición, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México.

Jorge Maldonado-Hernández (J)

Unidad de Investigación Médica en Nutrición, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México. Electronic address: jormh@yahoo.com.mx.

Leticia Sebastián-Medina (L)

Laboratorio de Nutrigenómica y Nutrigenética, Instituto Nacional de Medicina Genómica, Ciudad de México, México.

María Elizabeth Tejero-Barrera (ME)

Laboratorio de Nutrigenómica y Nutrigenética, Instituto Nacional de Medicina Genómica, Ciudad de México, México.

Ricardo Martín Robledo-Pérez (RM)

Laboratorio de Diagnóstico, Universidad Politécnica del Estado de Morelos, Cuernavaca, Morelos, México.

Salvador Villalpando-Hernández (S)

Centro de Investigación en Nutrición y Salud, Instituto Nacional de Salud Pública, Cuernavaca, Morelos, México.

Zobeida Analilia Ventura-Bravo (ZA)

Unidad de Investigación Médica en Nutrición, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México.

Laura Katia Morales-Ramírez (LK)

Unidad de Investigación Médica en Nutrición, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México.

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Classifications MeSH