Formation of a Human β-Cell Population within Pancreatic Islets Is Set Early in Life (original) (raw)

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1The Kovler Diabetes Center (B.E.G., P.C.M., D.D., B.A.H., C.J.R.), Chicago, Illinois 60637

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1The Kovler Diabetes Center (B.E.G., P.C.M., D.D., B.A.H., C.J.R.), Chicago, Illinois 60637

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1The Kovler Diabetes Center (B.E.G., P.C.M., D.D., B.A.H., C.J.R.), Chicago, Illinois 60637

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1The Kovler Diabetes Center (B.E.G., P.C.M., D.D., B.A.H., C.J.R.), Chicago, Illinois 60637

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2Department of Medicine,and Department of Pathology (M.L., A.H.), University of Chicago, Chicago, Illinois 60637

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2Department of Medicine,and Department of Pathology (M.L., A.H.), University of Chicago, Chicago, Illinois 60637

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3Department of Pathology, Immunology, and Laboratory Medicine (A.J.W., M.A.A.), University of Florida College of Medicine, Gainesville, Florida 32607

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3Department of Pathology, Immunology, and Laboratory Medicine (A.J.W., M.A.A.), University of Florida College of Medicine, Gainesville, Florida 32607

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1The Kovler Diabetes Center (B.E.G., P.C.M., D.D., B.A.H., C.J.R.), Chicago, Illinois 60637

*Address all correspondence and requests for reprints to: Christopher J. Rhodes, Ph.D., The Kovler Diabetes Center, University of Chicago, 900 East 57th Street, Chicago, Illinois 60637.

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Received:

24 January 2012

Published:

01 September 2012

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Brigid E. Gregg, Patrick C. Moore, Damien Demozay, Ben A. Hall, Mei Li, Aliya Husain, Amy J. Wright, Mark A. Atkinson, Christopher J. Rhodes, Formation of a Human β-Cell Population within Pancreatic Islets Is Set Early in Life, The Journal of Clinical Endocrinology & Metabolism, Volume 97, Issue 9, 1 September 2012, Pages 3197–3206, https://doi.org/10.1210/jc.2012-1206
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Context:

Insulin resistance can be compensated by increased functional pancreatic β-cell mass; otherwise, diabetes ensues. Such compensation depends not only on environmental and genetic factors but also on the baseline β-cell mass from which the expansion originates.

Objective:

Little is known about assembly of a baseline β-cell mass in humans. Here, we examined formation of β-cell populations relative to other pancreatic islet cell types and associated neurons throughout the normal human lifespan.

Design and Methods:

Human pancreatic sections derived from normal cadavers aged 24 wk premature to 72 yr were examined by immunofluorescence. Insulin, glucagon, and somatostatin were used as markers for β-, α-, and δ-cells, respectively. Cytokeratin-19 marked ductal cells, Ki67 cell proliferation, and Tuj1 (neuronal class III β-tubulin) marked neurons.

Results:

Most β-cell neogenesis was observed preterm with a burst of β-cell proliferation peaking within the first 2 yr of life. Thereafter, little indication of β-cell growth was observed. Postnatal proliferation of α- and δ-cells was rarely seen, but a wave of ductal cell proliferation was found mostly associated with exocrine cell expansion. The β-cell to α-cell ratio doubled neonatally, reflecting increased growth of β-cells, but during childhood, there was a 7-fold change in the β-cell to δ-cell ratio, reflecting an additional loss of δ-cells. A close association of neurons to pancreatic islets was noted developmentally and retained throughout adulthood. Negligible neuronal association to exocrine pancreas was observed.

Conclusion:

Human baseline β-cell population and appropriate association with other islet cell types is established before 5 yr of age.

Copyright © 2012 by The Endocrine Society

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