Variant rs17619600 in the gene encoding serotonin receptor 2B (HTR2B) increases the risk of gestational diabetes mellitus: a case-control study.


Journal

European journal of medical research
ISSN: 2047-783X
Titre abrégé: Eur J Med Res
Pays: England
ID NLM: 9517857

Informations de publication

Date de publication:
21 Jul 2023
Historique:
received: 13 10 2022
accepted: 05 07 2023
medline: 24 7 2023
pubmed: 22 7 2023
entrez: 21 7 2023
Statut: epublish

Résumé

During pregnancy, the increase in maternal insulin resistance is compensated by hyperplasia and increased function of maternal pancreatic beta cells; the failure of this compensatory mechanism is associated with gestational diabetes mellitus (GDM). Serotonin participates in beta cell adaptation, acting downstream of the prolactin pathway; the blocking of serotonin receptor B (HTR2B) signaling in pregnant mice impaired beta cell expansion and caused glucose intolerance. Thus, given the importance of the serotoninergic system for the adaptation of beta cells to the increased insulin demand during pregnancy, we hypothesized that genetic variants (single nucleotide polymorphisms [SNPs]) in the gene encoding HTR2B could influence the risk of developing GDM. This was a case-control study. Five SNPs (rs4973377, rs765458, rs10187149, rs10194776, and s17619600) in HTR2B were genotyped by real-time polymerase chain reaction in 453 women with GDM and in 443 pregnant women without GDM. Only the minor allele C of SNP rs17619600 conferred an increased risk for GDM in the codominant model (odds ratio [OR] 2.15; 95% confidence interval [CI] 1.53-3.09; P < 0.0001) and in the rare dominant model (OR 2.32; CI 1.61-3.37; P < 0.0001). No associations were found between the SNPs and insulin use, maternal weight gain, newborn weight, or the result of postpartum oral glucose tolerance test (OGTT). In the overall population, carriers of the XC genotype (rare dominant model) presented a higher area under the curve (AUC) of plasma glucose during the OGTT, performed for diagnostic purposes, compared with carriers of the TT genotype of rs17619600. SNP rs17619600 in the HTR2B gene influences glucose homeostasis, probably affecting insulin release, and the presence of the minor allele C was associated with a higher risk of GDM.

Sections du résumé

BACKGROUND BACKGROUND
During pregnancy, the increase in maternal insulin resistance is compensated by hyperplasia and increased function of maternal pancreatic beta cells; the failure of this compensatory mechanism is associated with gestational diabetes mellitus (GDM). Serotonin participates in beta cell adaptation, acting downstream of the prolactin pathway; the blocking of serotonin receptor B (HTR2B) signaling in pregnant mice impaired beta cell expansion and caused glucose intolerance. Thus, given the importance of the serotoninergic system for the adaptation of beta cells to the increased insulin demand during pregnancy, we hypothesized that genetic variants (single nucleotide polymorphisms [SNPs]) in the gene encoding HTR2B could influence the risk of developing GDM.
METHODS METHODS
This was a case-control study. Five SNPs (rs4973377, rs765458, rs10187149, rs10194776, and s17619600) in HTR2B were genotyped by real-time polymerase chain reaction in 453 women with GDM and in 443 pregnant women without GDM.
RESULTS RESULTS
Only the minor allele C of SNP rs17619600 conferred an increased risk for GDM in the codominant model (odds ratio [OR] 2.15; 95% confidence interval [CI] 1.53-3.09; P < 0.0001) and in the rare dominant model (OR 2.32; CI 1.61-3.37; P < 0.0001). No associations were found between the SNPs and insulin use, maternal weight gain, newborn weight, or the result of postpartum oral glucose tolerance test (OGTT). In the overall population, carriers of the XC genotype (rare dominant model) presented a higher area under the curve (AUC) of plasma glucose during the OGTT, performed for diagnostic purposes, compared with carriers of the TT genotype of rs17619600.
CONCLUSIONS CONCLUSIONS
SNP rs17619600 in the HTR2B gene influences glucose homeostasis, probably affecting insulin release, and the presence of the minor allele C was associated with a higher risk of GDM.

Identifiants

pubmed: 37480094
doi: 10.1186/s40001-023-01211-6
pii: 10.1186/s40001-023-01211-6
pmc: PMC10362639
doi:

Substances chimiques

Insulin 0
Receptor, Serotonin, 5-HT2B 0
HTR2B protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

243

Informations de copyright

© 2023. The Author(s).

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Auteurs

Juliana Regina Chamlian Zucare Penno (JRCZ)

Laboratório de Carboidratos e Radioimunoensaios (LIM-18), Hospital das Clínicas HCFMUSP, Universidade de São Paulo, Av. Dr. Arnaldo 455, Sala #3321, CEP, 01246-000, Sao Paulo, SP, Brazil.

Daniele Pereira Santos-Bezerra (DP)

Laboratório de Carboidratos e Radioimunoensaios (LIM-18), Hospital das Clínicas HCFMUSP, Universidade de São Paulo, Av. Dr. Arnaldo 455, Sala #3321, CEP, 01246-000, Sao Paulo, SP, Brazil.
Departamento de Fisiologia e Biofísica, Instituto de Ciências Biomédicas, Universidade de São Paulo, Av. Prof. Lineu Prestes 1524, Sao Paulo, SP, Brazil.

Ana Mercedes Cavaleiro (AM)

Laboratório de Carboidratos e Radioimunoensaios (LIM-18), Hospital das Clínicas HCFMUSP, Universidade de São Paulo, Av. Dr. Arnaldo 455, Sala #3321, CEP, 01246-000, Sao Paulo, SP, Brazil.

Ana Maria da Silva Sousa (AM)

Disciplina de Obstetrícia, Departamento de Obstetrícia e Ginecologia, Faculdade de Medicina FMUSP, Universidade de São Paulo, Instituto Central-Hospital das Clínicas, Av. Dr. Enéas de Carvalho Aguiar 255, 10º Andar, Sala 10.093, CEP, 05403-000, Sao Paulo, SP, Brazil.

Tatiana Assunção Zaccara (TA)

Disciplina de Obstetrícia, Departamento de Obstetrícia e Ginecologia, Faculdade de Medicina FMUSP, Universidade de São Paulo, Instituto Central-Hospital das Clínicas, Av. Dr. Enéas de Carvalho Aguiar 255, 10º Andar, Sala 10.093, CEP, 05403-000, Sao Paulo, SP, Brazil.

Rafaela Alkmin da Costa (RA)

Disciplina de Obstetrícia, Departamento de Obstetrícia e Ginecologia, Faculdade de Medicina FMUSP, Universidade de São Paulo, Instituto Central-Hospital das Clínicas, Av. Dr. Enéas de Carvalho Aguiar 255, 10º Andar, Sala 10.093, CEP, 05403-000, Sao Paulo, SP, Brazil.

Rossana Pulcineli Vieira Francisco (RPV)

Disciplina de Obstetrícia, Departamento de Obstetrícia e Ginecologia, Faculdade de Medicina FMUSP, Universidade de São Paulo, Instituto Central-Hospital das Clínicas, Av. Dr. Enéas de Carvalho Aguiar 255, 10º Andar, Sala 10.093, CEP, 05403-000, Sao Paulo, SP, Brazil.

Maria Lucia Correa-Giannella (ML)

Laboratório de Carboidratos e Radioimunoensaios (LIM-18), Hospital das Clínicas HCFMUSP, Universidade de São Paulo, Av. Dr. Arnaldo 455, Sala #3321, CEP, 01246-000, Sao Paulo, SP, Brazil. maria.giannella@fm.usp.br.

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