期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 103, 期 7, 页码 2334-2339出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0510790103
关键词
alpha cell; beta cell; cytoplasmic free Ca2+; concentration; insulin; glucagon
资金
- NCRR NIH HHS [M01 RR016587, IU42RR016603, U42 RR016603, M01RR16587, 5U42RR016603] Funding Source: Medline
- NIDDK NIH HHS [R03 DK075487, DK-58508, R01 DK058508, 1R01-DK55347] Funding Source: Medline
The cytoarchitecture of human islets has been examined, focusing on cellular associations that provide the anatomical framework for paracrine interactions. By using confocal microscopy and multiple immunofluorescence, we found that, contrary to descriptions of prototypical islets in textbooks and in the literature, human islets did not show anatomical subdivisions. Insulin-immunoreactive beta cells, glucagon-immunoreactive a cells, and somatostatin-containing delta cells were found scattered throughout the human islet. Human beta cells were not clustered, and most (71%) showed associations with other endocrine cells, suggesting unique paracrine interactions in human islets. Human islets contained proportionally fewer beta cells and more alpha cells than did mouse islets. In human islets, most beta, alpha, and delta cells were aligned along blood vessels with no particular order or arrangement, indicating that islet microcirculation likely does not determine the order of paracrine interactions. We further investigated whether the unique human islet cytoarchitecture had functional implications. Applying imaging of cytoplasmic free Ca2+ concentration, [Ca2+](i), we found that beta cell oscillatory activity was not coordinated throughout the human islet as it was in mouse islets. Furthermore, human islets responded with an increase in [Ca2+](i) when lowering the glucose concentration to 1 mM, which can be attributed to the large contribution of alpha cells to the islet composition. We conclude that the unique cellular arrangement of human islets has functional implications for islet cell function.
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