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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.

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Pharmacotherapy of type 1 diabetes - part 1: yesterday.

Expert Opin Pharmacother

January 2025

The Association of Diabetes Investigators, Newport Coast, CA, USA.

Introduction: Type 1 diabetes is a unique autoimmune attack on the β cell of the pancreatic islet resulting in progressive destruction of these cells and as a result the ability of the body to maintain insulin production. The consequences of insulin deficiency are very severe, and the disease was fatal prior to the ability to extract insulin from animal pancreas in 1921. We review progress in the treatment of childhood type 1 diabetes over the past 100 years.

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Autoimmune Type 1 Diabetes: An Early Approach Appraisal for Spain by the AGORA Diabetes Collaborative Group.

J Clin Med

January 2025

Clinical and Experimental Endocrinology, Department of Chronic Diseases and Metabolism (CHROMETA), KU Leuven, 3000 Leuven, Belgium.

Type 1 diabetes (T1D) is an autoimmune disorder characterized by the destruction of insulin-producing pancreatic beta-cells, leading to lifelong insulin dependence. This review explores the current understanding of T1D pathogenesis, clinical progression, and emerging therapeutic approaches. We examined the complex interplay between genetic predisposition and environmental factors that could trigger the autoimmune response as well as the immunological mechanisms involved in beta-cell destruction.

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Type 1 diabetes (T1D) is related to the autoimmune destruction of β-cells, leading to their almost complete absence in patients with longstanding T1D. However, endogenous insulin secretion persists in such patients as evidenced by the measurement of plasma C-peptide. Recently, a low level of insulin has been found in non-β islet cells of patients with longstanding T1D, indicating that other islet cell types may contribute to persistent insulin secretion.

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Decoding the Contribution of IAPP Amyloid Aggregation to Beta Cell Dysfunction: A Systematic Review and Epistemic Meta-Analysis of Type 1 Diabetes.

Int J Mol Sci

January 2025

Unidad de Investigación en Enfermedades Metabólicas, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City 06720, Mexico.

Diabetes Mellitus Type 1 (DM1) is an autoimmune disease characterized by the destruction of beta cells in the pancreas. Although amyloid formation has been well-studied in Diabetes Mellitus Type 2 (DM2), its role in DM1 remains unclear. Understanding how islet amyloid polypeptide (IAPP) contributes to beta cell dysfunction and death in DM1 could provide critical insights into disease mechanisms and pave the way for novel diagnostic and therapeutic strategies.

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