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Beta cell differentiation during early human pancreas development

Lookup NU author(s): Lee Turnpenny, Dr Stephen Ball, Dr David Wilson


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Understanding gene expression profiles during early human pancreas development is limited by comparison to studies in rodents. In this study, from the inception of pancreatic formation, embryonic pancreatic epithelial cells, approximately half of which were proliferative, expressed nuclear PDX1 and cytoplasmic CK19. Later, in the fetal pancreas, insulin was the most abundant hormone detected during the first trimester in largely non-proliferative cells. At sequential stages of early fetal development, as the number of insulin-positive cell clusters increased, the detection of CK19 in these cells diminished. PDX1 remained expressed in fetal beta cells. Vascular structures were present within the loose stroma surrounding pancreatic epithelial cells during embryogenesis. At 10 weeks post-conception (w.p.c.), all clusters containing more than ten insulin-positive cells had developed an intimate relationship with these vessels, compared with the remainder of the developing pancreas. At 12-13 w.p.c., human fetal islets, penetrated by vasculature, contained cells independently immunoreactive for insulin, glucagon, somatostatin and pancreatic polypeptide (PP), coincident with the expression of maturity markers prohormone convertase 1/3 (PC1/3), islet amyloid polypeptide, Chromogranin A and, more weakly, GLUT2. These data support the function of fetal beta cells as true endocrine cells by the end of the first trimester of human pregnancy. © 2004 Society for Endocrinology.

Publication metadata

Author(s): Piper K, Brickwood S, Turnpenny LW, Cameron IT, Ball SG, Wilson DI, Hanley NA

Publication type: Article

Publication status: Published

Journal: Journal of Endocrinology

Year: 2004

Volume: 181

Issue: 1

Pages: 11-23

ISSN (print): 0022-0795

ISSN (electronic): 1479-6805

Publisher: BioScientifica Ltd


DOI: 10.1677/joe.0.1810011

PubMed id: 15072563


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Funder referenceFunder name
G9826762Medical Research Council