New Advances in Insulin—100 Years Since Its Discovery: 2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 January 2026 | Viewed by 863

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Dear Colleagues,

The discovery of insulin in 1921 represented a milestone in the treatment of diabetes. In 1923, the Nobel Prize for Medicine was awarded for its discovery, and it was one of the most important discoveries in the history of medical science, affecting hundreds of millions of people worldwide. Thousands of lives have been saved, and the life expectancy of people with diabetes has been significantly extended. Since its discovery, insulin has been continuously improved through pharmacological development and optimized for therapeutic purposes, including the development of intermediate- and long-acting insulins, the ability to produce human insulin, and finally, the development of insulin analogs with improved properties using recombinant DNA technology.

Despite increasing awareness, diabetes is still one of the most challenging health problems in the 21st century. In the last 15 years, the number of people diagnosed with type 1 diabetes has increased by 45%, and the number of people diagnosed with type 2 diabetes has increased by 95%. Recently, the focus in the treatment of diabetes has been on new therapeutic options; however, insulin is still one of the most potent therapeutic options for patients with type 2 diabetes and is the only one for patients with type 1 diabetes.

Considering this context, this Special Issue will focus on the roles of insulin and insulin action in a broad sense. We welcome submissions related to new knowledge about insulin secretion and action, as well as the development and action of insulin analogs and their effects on glycemic control and chronic complications in diabetes.

Dr. Tomislav Bulum
Guest Editor

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Keywords

  • insulin action
  • insulin analogs
  • type 1 diabetes
  • type 2 diabetes
  • complications
  • glucose homeostasis

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Research

15 pages, 704 KB  
Article
Fetal Sex Modulates Hofbauer Cells’ Response to Diabetes in Human Placenta
by Zdenek Tauber, Max Mrstik, Adela Burianova, Katerina Koubova and Katerina Cizkova
Biomedicines 2025, 13(11), 2606; https://doi.org/10.3390/biomedicines13112606 - 24 Oct 2025
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Abstract
Background: Hofbauer cells (HBCs) are fetal-origin macrophages in the placental villous stroma that contribute to immune tolerance at the feto–maternal interface. They predominantly display an M2 phenotype, characterized by CD206 expression. Methods: Using immunohistochemistry and morphometric analysis, we quantified HBCs, assessed [...] Read more.
Background: Hofbauer cells (HBCs) are fetal-origin macrophages in the placental villous stroma that contribute to immune tolerance at the feto–maternal interface. They predominantly display an M2 phenotype, characterized by CD206 expression. Methods: Using immunohistochemistry and morphometric analysis, we quantified HBCs, assessed CD206 intensity and morphology, and evaluated apoptotic body accumulation in placental villi. Comparisons were made among pregnancies complicated by type 1 diabetes mellitus (T1DM), gestational diabetes mellitus (GDM), and normoglycemic controls, as well as between male and female fetuses. Results: Significant effects of maternal diabetes and fetal sex on CD206 intensity were observed ([diagnosis: F = 2773.00, p < 0.0001; sex: F = 12.19, p = 0.0005]), with a strong interaction (F = 165.40, p < 0.0001). In controls, CD206 intensity was higher in female than male fetuses (p < 0.0001). Across groups, CD206 intensity decreased progressively from controls to GDM and T1DM, with a more pronounced reduction in females. Reduced CD206 was associated with elongation and irregular HBC morphology and increased IL-1β (r = −0.392, p = 0.003; r = −0.609, p < 0.0001) suggesting less tolerogenic phenotype. For apoptotic bodies, significant main effects of maternal diabetes and fetal sex were detected ([diagnosis: F = 97.16, p < 0.0001; sex: F = 15.88, p = 0.0001]). Accumulation increased progressively from controls to GDM and T1DM, with higher counts in males. Conclusions: Maternal diabetes is associated with reduced CD206 intensity, altered HBC morphology, and accumulation of apoptotic bodies in placental villi. Our results suggest greater HBC plasticity, potentially contributing to a tolerogenic placental environment in females. Full article
(This article belongs to the Special Issue New Advances in Insulin—100 Years Since Its Discovery: 2nd Edition)
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