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J Clin Endocrinol Metab. 2017 Aug 1;102(8):2647-2659. doi: 10.1210/jc.2016-3806.

β Cells Persist in T1D Pancreata Without Evidence of Ongoing β-Cell Turnover or Neogenesis.

Author information

McNair Medical Institute, Pediatric Diabetes and Endocrinology, Baylor College of Medicine, Texas Children's Hospital, Houston, Texas 77030.
Division of Endocrinology and Diabetes, Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104.



The cellular basis of persistent β-cell function in type 1 diabetes (T1D) remains enigmatic. No extensive quantitative β-cell studies of T1D pancreata have been performed to test for ongoing β-cell regeneration or neogenesis.


We sought to determine the mechanism of β-cell persistence in T1D pancreata.


We studied T1D (n = 47) and nondiabetic control (n = 59) pancreata over a wide range of ages from the Juvenile Diabetes Research Foundation Network of Pancreatic Organ Donors with Diabetes via high-throughput microscopy.

Intervention and Main Outcome Measures:

We quantified β-cell mass, β-cell turnover [via Ki-67 and terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL)], islet ductal association, and insulin/glucagon coexpression in T1D and control pancreata.


Residual insulin-producing β cells were detected in some (but not all) T1D cases of varying disease duration. Several T1D pancreata had substantial numbers of β cells. Although β-cell proliferation was prominent early in life, it dramatically declined after infancy in both nondiabetic controls and T1D individuals. However, β-cell proliferation was equivalent in control and T1D pancreata. β-cell death (assessed by TUNEL) was extremely rare in control and T1D pancreata. Thus, β-cell turnover was not increased in T1D. Furthermore, we found no evidence of small islet/ductal neogenesis or α-cell to β-cell transdifferentiation in T1D pancreata, regardless of disease duration.


Longstanding β-cell function in patients with T1D appears to be largely a result of β cells that persist, without any evidence of attempted β-cell regeneration, small islet/ductal neogenesis, or transdifferentiation from other islet endocrine cell types.

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