Document Detail


Formation of a human β-cell population within pancreatic islets is set early in life.
MedLine Citation:
PMID:  22745242     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Brigid E Gregg; Patrick C Moore; Damien Demozay; Ben A Hall; Mei Li; Aliya Husain; Amy J Wright; Mark A Atkinson; Christopher J Rhodes
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-06-28
Journal Detail:
Title:  The Journal of clinical endocrinology and metabolism     Volume:  97     ISSN:  1945-7197     ISO Abbreviation:  J. Clin. Endocrinol. Metab.     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-09-10     Completed Date:  2012-11-26     Revised Date:  2014-04-08    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3197-206     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Aged
Autopsy
Biological Markers
Cell Count
Cell Proliferation
Child
Child, Preschool
Fluorescent Antibody Technique
Humans
Infant
Infant, Newborn
Infant, Premature
Insulin-Secreting Cells / physiology*
Islets of Langerhans / cytology*,  growth & development*
Middle Aged
Neurons / physiology
Pancreas, Exocrine / cytology
Pancreatic Hormones / analysis,  metabolism
Paraffin Embedding
Young Adult
Grant Support
ID/Acronym/Agency:
DK20595/DK/NIDDK NIH HHS; DK55267/DK/NIDDK NIH HHS; R01 DK055267/DK/NIDDK NIH HHS; UL1 TR000064/TR/NCATS NIH HHS
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Pancreatic Hormones
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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