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Epigenetic memory as crucial contributing factor in directing the differentiation of human iPSC into pancreatic β-cells in vitro.
Cell Tissue Res
January 2025
Diabetes Research Center, Qatar Biomedical Research Institute (QBRI), Qatar Foundation (QF), Hamad Bin Khalifa University (HBKU), Doha, Qatar.
Impaired insulin secretion contributes to the pathogenesis of type 1 diabetes mellitus through autoimmune destruction of pancreatic β-cells and the pathogenesis of severe forms of type 2 diabetes mellitus through β-cell dedifferentiation and other mechanisms. Replenishment of malfunctioning β-cells via islet transplantation has the potential to induce long-term glycemic control in the body. However, this treatment option cannot widely be implemented in clinical due to healthy islet donor shortage.
View Article and Find Full Text PDFHigh-Yield Generation of Glucose-Responsive Pseudoislets From Murine Insulinoma Cells for Studies and Longitudinal Monitoring of Graft Survival .
Cell Transplant
January 2025
Diabetes Research Institute, University of Miami Miller School of Medicine, Miami, FL, USA.
Compared to primary pancreatic islets, insulinoma cell-derived 3D pseudoislets offer a more accessible, consistent, renewable, and widely applicable model system for optimization and mechanistic studies in type 1 diabetes (T1D). Here, we report a simple and efficient method for generating 3D pseudoislets from MIN6 and NIT-1 murine insulinoma cells. These pseudoislets are homogeneous in size and morphology (~150 µm), exhibit functional glucose-stimulated insulin secretion (GSIS) up to 18 days (NIT-1) enabling long-term studies, are produced in high yield [>35,000 Islet Equivalence from 30 ml culture], and are suitable for both and studies, including for encapsulation studies.
View Article and Find Full Text PDFRisk Factors and Mechanisms for Diabetes in Pancreatitis.
Gastroenterol Clin North Am
March 2025
Department of Pediatrics, University of Minnesota, MMC 391, 420 Delaware Street Southeast, Minneapolis, MN 55455, USA. Electronic address:
Diabetes (DM) can occur as a complication of acute, acute recurrent, or chronic pancreatitis, affecting more than 30% of adults with chronic pancreatitis. Data on the pathophysiology and management are limited, especially in pediatric population. Proposed mechanisms include insulin deficiency, insulin resistance, decreased pancreatic polypeptide, and possible beta-cell autoimmunity (in a small subset).
View Article and Find Full Text PDFThe role of memory T cells in type 1 diabetes: Phenotypes, mechanisms, and therapeutic implications.
Autoimmun Rev
January 2025
Trauma Research Center, Shahid Rajaee (Emtiaz) Trauma Hospital, Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address:
Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by the loss of insulin-producing cells in the pancreatic islets. Patients with T1D have autoreactive CD4 and CD8 T cells that show specific features, indicating previous exposure to self-antigens. Despite that memory T cells are vital components of the adaptive immune system, providing enduring protection against pathogens; individuals with T1D have a higher proportion of memory T cells compared to healthy individuals with naїve phenotypes.
View Article and Find Full Text PDFIntroduction: Type 1 diabetes is often accompanied by autoimmune thyroid disease. We aimed to investigate the clinical characteristics of Japanese patients with acute-onset type 1 diabetes and thyroid autoantibodies, focusing on decreased endogenous insulin secretion.
Materials And Methods: We examined 80 patients with acute-onset type 1 diabetes, classifying them into two groups with and without thyroid autoantibodies and compared the clinical characteristics of the two groups.
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