The associations of incretin hormone concentration with gestational diabetes mellitus

Background: Enteropancreatic hormonal system disorder is a possible reason for β-cell dysfunction and carbohydrate metabolism disorder among pregnant women. However, no information is available about the state of enteroinsulin hormones [glucagon, glucose-dependent insulinotropic peptide (GIP), gluca...

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Autores principales: Tatiana V. Saprina, Ekaterina S. Timokhina, Olga K. Goncharevich, Svetlana V. Budeeva, Tatiana S. Prokhorenko, Lyubov A. Tashireva, Nadezhda N. Musina, Irina V. Dronova
Formato: article
Lenguaje:EN
RU
Publicado: Endocrinology Research Centre 2016
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Acceso en línea:https://doaj.org/article/152a9f78f6864022a6056a32d20297ce
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Sumario:Background: Enteropancreatic hormonal system disorder is a possible reason for β-cell dysfunction and carbohydrate metabolism disorder among pregnant women. However, no information is available about the state of enteroinsulin hormones [glucagon, glucose-dependent insulinotropic peptide (GIP), glucagon-like peptide1 (GLP-1) and GLP-2] during pregnancy. The role of enteroinsulin hormones in the development of carbohydrate metabolism disorder during pregnancy is poorly understood. Aim: To quantify and compare incretin hormone secretion in groups of pregnant women with and without gestational diabetes mellitus (GDM). Materials and methods: The study included 80 patients, 50 of whom had GDM, and the control group consisted of 30 pregnant women without GDM. All patients underwent an oral glucose tolerance test; glycated haemoglobin (HbA1c) estimation; ferritin, transferrin, basal and postprandial glucagon estimation; GLP-1 and GLP-2 estimation. Results: Basal glucagon and GLP-1 levels were significantly higher (p <0. 05) in the group of women with GDM than in the control group. The most significant differences in GLP-1, basal and postprandial glucagon levels were observed during the first trimester of pregnancy. Conclusion: High GLP-1 levels in the group of women with GDM may reflect a state of ‘incretin resistance’, which is similar to hyperinsulinemia in the early stages of type 2 diabetes mellitus.