REVIEW article
Front. Endocrinol.
Sec. Clinical Diabetes
Volume 16 - 2025 | doi: 10.3389/fendo.2025.1663643
Autoimmune pathogenesis of gestational diabetes mellitus: the risk of progression to type 1 diabetes mellitus
Provisionally accepted- 1Polish Mother’s Memorial Hospital Research Institute, Łódź, Poland
- 2Fakultni nemocnice Hradec Kralove, Hradec Kralove, Czechia
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Gestational diabetes mellitus (GDM) is one of the most commonly diagnosed metabolic disorders in pregnancy, affecting between 5% and 20% of patients worldwide, depending on the diagnostic criteria and population. Although GDM pathogenesis is predominantly based on insulin resistance mechanisms resulting from the influence of pregnancy hormones, an increasing number of studies point to a significant role of immunological factors in the process of GDM development. In some GDM patients, autoantibodies targeting pancreatic beta cells are detected. Consequently, autoimmune processes may constitute an important element of GDM etiology, particularly in cases where GDM is a transitive condition leading to type 1 diabetes mellitus (T1DM) after the pregnancy. Disorders causing the destruction of beta cells within the pancreas precipitate permanent hyperglycemia in patients with autoimmune GDM (gestational diabetes mellitus with autoantibodies). characteristics. Genetic factors also play a significant role in this process, including single-nucleotide polymorphisms associated with the tissue compatibility system, such as HLA, CTLA-4, PTPN22 and IL2RA, which cause predisposition to T1DM. The following article discusses the current state of knowledge and presents GDM pathogenesis from the standpoint of immune mechanisms capable of affecting the development of this condition. It discusses potential markers that may help identify GDM patients at risk of progressing to permanent diabetes mellitus as well as possible diagnostic and therapeutic strategies based on the latest findings.
Keywords: GDM, T1DM, Islet autoantibodies, Beta-cell dysfunction, Immune dysregulation
Received: 10 Jul 2025; Accepted: 12 Sep 2025.
Copyright: © 2025 Skibińska, Kacerovsky, Grzesiak and Wujcicka. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Milena Skibińska, milena.skibinska@gmail.com
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