Reversing pancreatic β-cell dedifferentiation in the treatment of type 2 diabetes

Exp Mol Med. 2023 Aug;55(8):1652-1658. doi: 10.1038/s12276-023-01043-8. Epub 2023 Aug 1.

Abstract

The maintenance of glucose homeostasis is fundamental for survival and health. Diabetes develops when glucose homeostasis fails. Type 2 diabetes (T2D) is characterized by insulin resistance and pancreatic β-cell failure. The failure of β-cells to compensate for insulin resistance results in hyperglycemia, which in turn drives altered lipid metabolism and β-cell failure. Thus, insulin secretion by pancreatic β-cells is a primary component of glucose homeostasis. Impaired β-cell function and reduced β-cell mass are found in diabetes. Both features stem from a failure to maintain β-cell identity, which causes β-cells to dedifferentiate into nonfunctional endocrine progenitor-like cells or to trans-differentiate into other endocrine cell types. In this regard, one of the key issues in achieving disease modification is how to reestablish β-cell identity. In this review, we focus on the causes and implications of β-cell failure, as well as its potential reversibility as a T2D treatment.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't
  • Research Support, N.I.H., Extramural

MeSH terms

  • Cell Dedifferentiation
  • Diabetes Mellitus, Type 2* / metabolism
  • Glucose / metabolism
  • Humans
  • Insulin / metabolism
  • Insulin Resistance*
  • Insulin-Secreting Cells* / metabolism

Substances

  • Insulin
  • Glucose