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Am J Physiol Endocrinol Metab 297: E323-E330, 2009. First published May 26, 2009; doi:10.1152/ajpendo.00284.2009
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Dynamics of β-cell turnover: evidence for β-cell turnover and regeneration from sources of β-cells other than β-cell replication in the HIP rat

Erica Manesso,1,2 Gianna M. Toffolo,1 Yoshifumi Saisho,2 Alexandra E. Butler,2 Aleksey V. Matveyenko,2 Claudio Cobelli,1 and Peter C. Butler2

1Department of Information Engineering, University of Padua, Padua, Italy; and 2Larry Hillblom Islet Research Center at David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California

Submitted 1 May 2009 ; accepted in final form 26 May 2009

Type 2 diabetes is characterized by hyperglycemia, a deficit in β-cells, increased β-cell apoptosis, and islet amyloid derived from islet amyloid polypeptide (IAPP). These characteristics are recapitulated in the human IAPP transgenic (HIP) rat. We developed a mathematical model to quantify β-cell turnover and applied it to nondiabetic wild type (WT) vs. HIP rats from age 2 days to 10 mo to establish 1) whether β-cell formation is derived exclusively from β-cell replication, or whether other sources of β-cells (OSB) are present, and 2) to what extent, if any, there is attempted β-cell regeneration in the HIP rat and if this is through β-cell replication or OSB. We conclude that formation and maintenance of adult β-cells depends largely (~80%) on formation of β-cells independent from β-cell duplication. Moreover, this source adaptively increases in the HIP rat, implying attempted β-cell regeneration that substantially slows loss of β-cell mass.

human islet amyloid polypeptide; diabetes mellitus; mathematical model


Address for reprint requests and other correspondence: P. C. Butler, Larry Hillblom Islet Research Center at David Geffen School of Medicine, UCLA, 900 Weyburn Place #A, Los Angeles, CA 90024-2852 (e-mail: pbutler{at}mednet.ucla.edu)






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