Death versus dedifferentiation: The molecular bases of beta cell mass reduction in type 2 diabetes.

  title={Death versus dedifferentiation: The molecular bases of beta cell mass reduction in type 2 diabetes.},
  author={Tong Sun and Xiao Han},
  journal={Seminars in cell \& developmental biology},
  • Tong SunXiao Han
  • Published 9 December 2019
  • Medicine, Biology
  • Seminars in cell & developmental biology

A Brief Review of the Mechanisms of β-Cell Dedifferentiation in Type 2 Diabetes

A better understanding of β- cell dedifferentiation process will help to identify novel therapeutic targets to prevent and/or reverse β-cell loss in type 2 diabetes.

MicroRNA Sequences Modulated by Beta Cell Lipid Metabolism: Implications for Type 2 Diabetes Mellitus

This review sought to identify the microRNA sequences regulated by metabolic challenges in beta cells and islets, their targets, highlight their function and assess their possible relevance as biomarkers of disease progression in diabetic individuals.

The Plasticity of Pancreatic β-Cells

Novel treatment(s) for diabetes targeting islet cell plasticity is outlined, such as transdifferentiation of pancreatic β-cell to α-cell and vice versa, because islet cells can exhibit plasticity, and they may have the ability to redifferentiate into any cell type.

Targeting β-cell dedifferentiation and transdifferentiation: opportunities and challenges

It is explored the possibility that there might be a time interval from the onset of β-cell dysfunction caused by dedifferentiation to the development of diabetes, which may offer a therapeutic window to reduce β- cell injury and to stabilize functionality.

Long Non-Coding RNAs as Key Modulators of Pancreatic β-Cell Mass and Function

An overview of the roles of lncRNAs in maintaining β-function and mass is provided, and their relevance in the development of diabetes is discussed.

Relationship Between Insulin-Receptor Substrate 1 and Langerhans’ Islet in a Rat Model of Type 2 Diabetes Mellitus

The reduction of IRS1 was weakly correlated with the destruction of Langerhans’ islets, suggesting there is an intermediate step between both parameters.

NGBR is required to ameliorate type 2 diabetes in mice by enhancing insulin sensitivity

Morus alba L. (Sangzhi) Alkaloids Promote Insulin Secretion, Restore Diabetic β-Cell Function by Preventing Dedifferentiation and Apoptosis

SZ-A alleviated hyperglycemia and glucose intolerance in type 2 diabetic KKAy mice and improved the function and morphology of diabetic islets and promotes insulin secretion in islet β cells and ameliorates β-cell dysfunction and mass reduction under diabetic conditions both in vivo and in vitro.



Pancreatic β Cell Mass Death

Evidence that β cell development and mass formation are guided by specific signaling systems, particularly hormones, transcription factors, and growth factors, all of which could be manipulated to enhance mass growth is discussed.

Evidence of β-Cell Dedifferentiation in Human Type 2 Diabetes.

The data support the view that pancreatic β-cells become dedifferentiated and convert to α- and δ-"like" cells in human type 2 diabetes, and should prompt a reassessment of goals in the prevention and treatment of β-cell dysfunction.

Beta‐Cell Dedifferentiation in Type 2 Diabetes: Concise Review

This study evaluated the evidence for β‐cell dedifferentiation in T2D, and T1D and examined experimental systems in which its mechanisms may be studied and concluded that prevention or induction of cell redifferentiation is needed for restoration of the functional β‐ cell mass.

Apoptosis in pancreatic β-islet cells in Type 2 diabetes.

  • T. Tomita
  • Biology, Medicine
    Bosnian journal of basic medical sciences
  • 2016
Animal models using knockout mice will shed light on the basic understanding of the pathophysiology of diabetes as a glucose metabolic disease complex, on the balance of anti-apoptotic Bcl family and pro-APoptotic genes, and will lead to eventual prevention and therapeutic application for T2DM with improving medications.

High glucose causes apoptosis in cultured human pancreatic islets of Langerhans: a potential role for regulation of specific Bcl family genes toward an apoptotic cell death program.

Comparing the effect of 5 days' culture in high glucose concentration versus normal glucose levels or hyperosmolar control on the survival of human pancreatic islets suggests that in human islets, high glucose may modulate the balance of proapoptotic and antiap optotic Bcl proteins toward apoptosis, thus favoring beta-cell death.

β-cell dysfunction: Its critical role in prevention and management of type 2 diabetes.

  • Y. Saisho
  • Medicine, Biology
    World journal of diabetes
  • 2015
Reducing β-cell workload appears to be the most effective way to preserve β- cell functional mass to date, underpinning the importance of lifestyle modification and weight loss for the treatment and prevention of T2DM.

β-Cell Deficit and Increased β-Cell Apoptosis in Humans With Type 2 Diabetes

Since the major defect leading to a decrease in β-cell mass in type 2 diabetes is increased apoptosis, while new islet formation andβ-cell replication are normal, therapeutic approaches designed to arrest apoptosis could be a significant new development in the management of type 2 Diabetes.

Mechanisms of β-cell dedifferentiation in diabetes: recent findings and future research directions.

The role of Foxo1, Myc and inhibitor of differentiation proteins are discussed, the emerging role of non-coding RNAs are highlighted and a novel hypothesis of β-cell dedifferentiation as a potential adaptive mechanism to escape cell death under stress conditions is proposed.

&bgr;-Cell Dedifferentiation in Patients With T2D With Adequate Glucose Control and Nondiabetic Chronic Pancreatitis

The data support the view that pancreatic β-cells are dedifferentiated in patients with T2D with adequate glucose control and suggest that inflammation-induced β-cell dedifferentiation can be a cause of pancreatogenic diabetes during disease progress.