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Islet Studies

β-Cell Deficit and Increased β-Cell Apoptosis in Humans With Type 2 Diabetes

  1. Alexandra E. Butler1,
  2. Juliette Janson2,
  3. Susan Bonner-Weir3,
  4. Robert Ritzel1,
  5. Robert A. Rizza4 and
  6. Peter C. Butler1
  1. 1Division of Endocrinology and Diabetes, Keck School of Medicine, University of Southern California, Los Angeles, California
  2. 2Karolinska Institute, Stockholm, Sweden
  3. 3Joslin Diabetes Center, Boston, Massachusetts
  4. 4Division of Endocrinology, Mayo Clinic, Rochester, Minnesota
    Diabetes 2003 Jan; 52(1): 102-110. https://doi.org/10.2337/diabetes.52.1.102
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    Article Information

    vol. 52 no. 1 102-110
    DOI 
    https://doi.org/10.2337/diabetes.52.1.102
    PubMed 
    12502499

    Published By 
    American Diabetes Association
    Print ISSN 
    0012-1797
    Online ISSN 
    1939-327X
    History 
    • Published in print January 1, 2003.

    Copyright & Usage 
    DIABETES

    Author Information

    1. Alexandra E. Butler1,
    2. Juliette Janson2,
    3. Susan Bonner-Weir3,
    4. Robert Ritzel1,
    5. Robert A. Rizza4 and
    6. Peter C. Butler1
    1. 1Division of Endocrinology and Diabetes, Keck School of Medicine, University of Southern California, Los Angeles, California
    2. 2Karolinska Institute, Stockholm, Sweden
    3. 3Joslin Diabetes Center, Boston, Massachusetts
    4. 4Division of Endocrinology, Mayo Clinic, Rochester, Minnesota
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      January 2003, 52(1)
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      β-Cell Deficit and Increased β-Cell Apoptosis in Humans With Type 2 Diabetes
      Alexandra E. Butler, Juliette Janson, Susan Bonner-Weir, Robert Ritzel, Robert A. Rizza, Peter C. Butler
      Diabetes Jan 2003, 52 (1) 102-110; DOI: 10.2337/diabetes.52.1.102

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      β-Cell Deficit and Increased β-Cell Apoptosis in Humans With Type 2 Diabetes
      Alexandra E. Butler, Juliette Janson, Susan Bonner-Weir, Robert Ritzel, Robert A. Rizza, Peter C. Butler
      Diabetes Jan 2003, 52 (1) 102-110; DOI: 10.2337/diabetes.52.1.102
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      • Acyl-Ghrelin Influences Pancreatic β-Cell Function by Interference with KATP Channels
      • Pancreatic β-Cell–Specific Deletion of VPS41 Causes Diabetes Due to Defects in Insulin Secretion
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