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Diabetes 53:S16-S21, 2004
© 2004 by the American Diabetes Association, Inc.

Section I: Insulin Resistance-Beta-Cell Connection in Type 2 Diabetes

Five Stages of Evolving Beta-Cell Dysfunction During Progression to Diabetes

Gordon C. Weir, and Susan Bonner-Weir

From the Section on Islet Transplantation and Cell Biology, Joslin Diabetes Center, Boston, Massachusetts

This article proposes five stages in the progression of diabetes, each of which is characterized by different changes in ß-cell mass, phenotype, and function. Stage 1 is compensation: insulin secretion increases to maintain normoglycemia in the face of insulin resistance and/or decreasing ß-cell mass. This stage is characterized by maintenance of differentiated function with intact acute glucose-stimulated insulin secretion (GSIS). Stage 2 occurs when glucose levels start to rise, reaching ~5.0–6.5 mmol/l; this is a stable state of ß-cell adaptation with loss of ß-cell mass and disruption of function as evidenced by diminished GSIS and ß-cell dedifferentiation. Stage 3 is a transient unstable period of early decompensation in which glucose levels rise relatively rapidly to the frank diabetes of stage 4, which is characterized as stable decompensation with more severe ß-cell dedifferentiation. Finally, stage 5 is characterized by severe decompensation representing a profound reduction in ß-cell mass with progression to ketosis. Movement across stages 1–4 can be in either direction. For example, individuals with treated type 2 diabetes can move from stage 4 to stage 1 or stage 2. For type 1 diabetes, as remission develops, progression from stage 4 to stage 2 is typically found. Delineation of these stages provides insight into the pathophysiology of both progression and remission of diabetes.

Address correspondence and reprint requests to Gordon C. Weir, MD, Section on Islet Transplantation and Cell Biology, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215. E-mail: gordon.weir{at}joslin.harvard.edu


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