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

@article{Sun2019DeathVD,
  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},
  year={2019}
}
  • 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

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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.

References

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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.

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&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.
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