The Role of Beta Cell Recovery in Type 2 Diabetes Remission

Int J Mol Sci. 2022 Jul 4;23(13):7435. doi: 10.3390/ijms23137435.

Abstract

Type 2 diabetes (T2D) has been considered a relentlessly worsening disease, due to the progressive deterioration of the pancreatic beta cell functional mass. Recent evidence indicates, however, that remission of T2D may occur in variable proportions of patients after specific treatments that are associated with recovery of beta cell function. Here we review the available information on the recovery of beta cells in (a) non-diabetic individuals previously exposed to metabolic stress; (b) T2D patients following low-calorie diets, pharmacological therapies or bariatric surgery; (c) human islets isolated from non-diabetic organ donors that recover from "lipo-glucotoxic" conditions; and (d) human islets isolated from T2D organ donors and exposed to specific treatments. The improvement of insulin secretion reported by these studies and the associated molecular traits unveil the possibility to promote T2D remission by directly targeting pancreatic beta cells.

Keywords: bariatric surgery; glucotoxicity; insulin secretion; lipotoxicity; low-calorie diets; pancreatic beta cells; pancreatic islets; remission; transcriptome; type 2 diabetes.

Publication types

  • Review

MeSH terms

  • Diabetes Mellitus, Type 2* / metabolism
  • Humans
  • Insulin / metabolism
  • Insulin Secretion
  • Insulin-Secreting Cells* / metabolism

Substances

  • Insulin

Grants and funding

This work has been supported by: the European Union’s Horizon 2020 research and innovation program T2Dsystems under grant agreement no. 667191; the Innovative Medicines Initiative 2 Joint Undertaking under grant agreements No 115,797 (INNODIA) and 945,268 (INNODIA HARVEST) (these Joint Undertakings receive support from the Union’s Horizon 2020 research and innovation program and “EFPIA”, “JDRF” and “The Leona M. and Harry B. Helmsley Charitable Trust”; the Italian Ministry of University and Research, PRIN 2017 (2017KAM2R5_005).