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Perspectives in Care

The Time Is Right for a New Classification System for Diabetes: Rationale and Implications of the β-Cell–Centric Classification Schema

  1. Stanley S. Schwartz1⇑,
  2. Solomon Epstein2,
  3. Barbara E. Corkey3,
  4. Struan F.A. Grant4,
  5. James R. Gavin III5 and
  6. Richard B. Aguilar6
  1. 1Main Line Health, Wynnewood, PA, and University of Pennsylvania, Philadelphia, PA
  2. 2Division of Endocrinology, Diabetes and Bone Disease, Department of Medicine, Mount Sinai Hospital, New York, NY
  3. 3Department of Medicine, Boston University School of Medicine, Boston, MA
  4. 4Division of Human Genetics and Center for Applied Genomics, Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA
  5. 5Emory University School of Medicine, Atlanta, GA
  6. 6Diabetes Nation, Sisters, OR
  1. Corresponding author: Stanley S. Schwartz, stschwar{at}gmail.com.
Diabetes Care 2016 Feb; 39(2): 179-186. https://doi.org/10.2337/dc15-1585
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    Figure 1

    Qualitative illustration of the spectrum of factors associated with different forms of DM, including the variable age at onset, lack of obesity, metabolic syndrome, genetic associations, different forms of immune changes, C-peptide secretion, and the need for insulin therapy. T1DM, type 1 DM; T2DM, type 2 diabetes. Adapted with permission from Leslie et al. (1).

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    Figure 2

    Genetic determinants influence IR (whether centrally or peripherally induced), loss of β-cell function and mass, environmental triggers (such as viruses, endocrine disruptors, food advanced glycosylation end products, gut biome), and immune modulation and inflammation. Singly or, more commonly, in various combinations, these factors converge on the genetically susceptible β-cell, impinge on β-cell function and biology, and orchestrate the shift from normoglycemia to hyperglycemia. As this process takes place regardless of subtype of DM, the dysfunctional β-cell is the final common denominator in all DM.

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    Figure 3

    β-Cell–centric construct: the egregious eleven. Dysfunction of the β-cells is the final common denominator in DM. A: Eleven currently known mediating pathways of hyperglycemia are shown. Many of these contribute to β-cell dysfunction (liver, muscle, adipose tissue [shown in red to depict additional association with IR], brain, colon/biome, and immune dysregulation/inflammation [shown in blue]), and others result from β-cell dysfunction through downstream effects (reduced insulin, decreased incretin effect, α-cell defect, stomach/small intestine via reduced amylin, and kidney [shown in green]). B: Current targeted therapies for each of the current mediating pathways of hyperglycemia. GLP-1, glucagon-like peptide 1; QR, quick release.

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Diabetes Care: 39 (2)

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February 2016, 39(2)
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The Time Is Right for a New Classification System for Diabetes: Rationale and Implications of the β-Cell–Centric Classification Schema
Stanley S. Schwartz, Solomon Epstein, Barbara E. Corkey, Struan F.A. Grant, James R. Gavin, Richard B. Aguilar
Diabetes Care Feb 2016, 39 (2) 179-186; DOI: 10.2337/dc15-1585

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The Time Is Right for a New Classification System for Diabetes: Rationale and Implications of the β-Cell–Centric Classification Schema
Stanley S. Schwartz, Solomon Epstein, Barbara E. Corkey, Struan F.A. Grant, James R. Gavin, Richard B. Aguilar
Diabetes Care Feb 2016, 39 (2) 179-186; DOI: 10.2337/dc15-1585
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