Open AccessIn Situ Analysis Reveals That CFTR Is Expressed in Only a Small Minority of β-Cells in Normal Adult Human Pancreas
Author(s) -
Michael G. White,
Rashmi R Maheshwari,
Scott Anderson,
Rolando BerlinguerPalmini,
Claire Jones,
Sarah J. Richardson,
Pavana G. Rotti,
Sarah Armour,
Yuchun Ding,
Natalio Krasnogor,
John F. Engelhardt,
Michael A. Gray,
Noel G. Morgan,
James Shaw
Publication year - 2019
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/clinem/dgz209
Subject(s) - cystic fibrosis transmembrane conductance regulator , cystic fibrosis , pathogenesis , diabetes mellitus , cystic fibrosis related diabetes , pancreas , secretion , cell , endocrinology , biology , medicine , regulator , microbiology and biotechnology , type 2 diabetes , impaired glucose tolerance , genetics , gene
Although diabetes affects 40% to 50% of adults with cystic fibrosis, remarkably little is known regarding the underlying mechanisms leading to impaired pancreatic β-cell insulin secretion. Efforts toward improving the functional β-cell deficit in cystic fibrosis-related diabetes (CFRD) have been hampered by an incomplete understanding of whether β-cell function is intrinsically regulated by cystic fibrosis transmembrane conductance regulator (CFTR). Definitively excluding meaningful CFTR expression in human β-cells in situ would contribute significantly to the understanding of CFRD pathogenesis.
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