Targeting beta-cell preservation in the management of type 2 diabetes

Authors

  • Charlotte K Boughton King’s College Hospital NHS Foundation Trust, London
  • Neil Munro University of Surrey
  • Martin Whyte King’s College Hospital NHS Foundation Trust, London and University of Surrey

DOI:

https://doi.org/10.15277/bjd.2017.148

Keywords:

type 2 diabetes (T2D), beta-cell function, remission

Abstract

Type 2 diabetes (T2D) is widely considered a chronic and progressive disease without cure. As beta-cell function progressively declines over time, blood glucose rises. Current management of T2D involves incremental introduction of dietary and drug therapies to achieve normoglycaemia. However, recent studies have demonstrated remission of T2D following bariatric surgery, very low calorie diet or intensive insulin therapy, raising the possibility that the declining beta-cell function in T2D may be arrested or even reversed. The point at which such interventions are introduced in the course of T2D is key for clinical benefit. Future treatment strategies should be revised to target early beta-cell preservation and thus disease remission. This article reviews the pathogenesis of beta-cell dysfunction and evidence for the clinical benefit of preserving beta-cell function in T2D, and discusses the evidence for beta-cell preservation of current glucose-lowering therapies with particular reference to their effect when initiated at the time of diagnosis of T2D.

Author Biographies

Charlotte K Boughton, King’s College Hospital NHS Foundation Trust, London

NIHR Academic Clinical Fellow and Diabetes and Endocrinology Registrar

Neil Munro, University of Surrey

Visiting Professor in Primary Care Diabetes

Martin Whyte, King’s College Hospital NHS Foundation Trust, London and University of Surrey

Clinical Senior Lecturer in Metabolic Medicine and Consultant Diabetes

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2017-12-15

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