Aos pacientes que participaram da pesquisa.À minha orientadora Dra. Maria Lúcia Cardillo Corrêa Giannella (Dra. Malu), agradeço por ter acreditado no meu sonho e me apoiado nessa jornada.Muito obrigada por ter aguentado todas as minhas inseguranças, minhas três gestações, a pandemia ... você sempre com palavras de calma e apoio, mostrando que conseguiríamos fazer tudo, sempre tão positiva, mostrando os caminhos que muitas vezes eu não conseguia ver. Obrigada por ser tão compreensiva e paciente com as minhas ansiedades.Agradeço à minha coorientadora, Rossana Pulcineli Vieira Francisco, por acreditar no nosso projeto, por me abrir as portas da Obstetrícia, por me acolher tão bem, quantos ensinamentos nessa área ao longo desses anos.Agradeço ao acolhimento que recebi da Obstetrícia, começando pela Lucinda Cristina Pereira, com a sua infinita gentileza, sempre tão disponível e pronta a ajudar. A enfermeira Ana Maria Sousa, com seu enorme sorriso me ajudou nas coletas dos pacientes, não conseguiria sem sua ajuda.Agradeço aos residentes e preceptores da Obstetrícia que acompanhavam os atendimentos das pacientes do estudo.
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 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 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 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.
Background 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 HTR2B gene could influence the risk of developing gestational diabetes mellitus (GDM). 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 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 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.
Background Given the importance of the serotoninergic system for the adaptation of beta cells to the increased insulin demand during pregnancy, we hypothesized that genetic variations (single nucleotide polymorphisms [SNPs]) in the HTR2B gene could influence the risk of developing gestational diabetes mellitus (GDM). 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 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 The presence of the rare allele C in the SNP rs17619600 in HTR2B gene increased the risk of GDM.
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