The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Beta-cell proliferation and apoptosis in the developing normal human pancreas and in hyperinsulinism of infancy.
Open accessAbstract
Hyperinsulinism of infancy (HI), also known as persistent hyperinsulinemic hypoglycemia of infancy, is a rare genetic disorder that occurs in approximately 1 of 50,000 live births. Histologically, pancreases from HI patients can be divided into 2 major groups. In the first, diffuse HI, beta-cell distribution is similar to that seen in normal neonatal pancreas, whereas in the second, focal HI, there is a discrete region of beta-cell adenomatous hyperplasia. In most patients, the clinical course of the disease suggests a slow progressive loss of beta-cell function. Using double immunostaining, we examined the proportion of beta-cells undergoing proliferation and apoptosis during the development of the normal human pancreas and in pancreases from diffuse and focal HI patients. In the control samples, our findings show a progressive decrease in beta-cell proliferation from 3.2 +/- 0.5% between 17 and 32 weeks of gestation to 0.13 +/- 0.08% after 6 months of age. In contrast, frequency of apoptosis is low (0.6 +/- 0.2%) in weeks 17-32 of gestation, elevated (1.3 +/- 0.3% ) during the perinatal period, and again low (0.08 +/- 0.3%) after 6 months of age. HI beta-cells showed an increased frequency of proliferation, with focal lesions showing particularly high levels. Similarly, the proportion of apoptotic cells was increased in HI, although this reached statistical significance only after 3 months of age. In conclusion, we demonstrated that islet remodeling normally seen in the neonatal period may be primarily due to a wave of beta-cell apoptosis that occurs at that time. In HI, our findings of persistently increased beta-cell proliferation and apoptosis provide a possible mechanism to explain the histologic picture seen in diffuse disease. The slow progressive decrease in insulin secretion seen clinically in these patients suggests that the net effect of these phenomena may be loss of beta-cell mass.
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Thomas, P. M., Cote, G. J., Wohllk, N., Haddad, B., Mathew, P. M., Rabl, W., Aguilar-Bryan, L., Gagel, R. F., & Bryan, J. (1995) · Science · doi:10.1126/science.7716548 · Cited by 806
Cited by
Meier, J. J., Butler, A. E., Saisho, Y., Monchamp, T., Galasso, R., Bhushan, A., Rizza, R. A., & Butler, P. C. (2008) · Diabetes · doi:10.2337/db07-1369 · Cited by 683
Regulation of pancreatic beta-cell mass
Bouwens, L., & Rooman, I. (2005) · Physiological Reviews · doi:10.1152/physrev.00025.2004 · Cited by 411
Formation of a human β-cell population within pancreatic islets is set early in life
Gregg, B. E., Moore, P. C., Demozay, D., Hall, B. A., Li, M., Husain, A., Wright, A. J., Atkinson, M. A., & Rhodes, C. J. (2012) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2012-1206 · Cited by 344
Hyperinsulinism in Infancy: From Basic Science to Clinical Disease
DUNNE, M. J., COSGROVE, K. E., SHEPHERD, R. M., AYNSLEY-GREEN, A., & LINDLEY, K. J. (2004) · Physiological Reviews · doi:10.1152/physrev.00022.2003 · Cited by 294
The replication of β cells in normal physiology, in disease and for therapy
Butler, P. C., Meier, J. J., Butler, A. E., & Bhushan, A. (2007) · Nature Clinical Practice Endocrinology & Metabolism · doi:10.1038/ncpendmet0647 · Cited by 268
Metadata
- Authors
- Kassem, S. A., Ariel, I., Thornton, P. S., Scheimberg, I., & Glaser, B.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2000-08-01
- Volume
- 49
- Issue
- 8
- Pages
- 1325-1333
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2060743272
- Cited by
- 361
- References
- 1
- FWCI
- 8.54
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Kassem, S. A., Ariel, I., Thornton, P. S., Scheimberg, I., & Glaser, B. (2000). Beta-cell proliferation and apoptosis in the developing normal human pancreas and in hyperinsulinism of infancy. Diabetes. https://doi.org/10.2337/diabetes.49.8.1325
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