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Restoring a functional β‐cell mass in diabetes
Author(s) -
Pipeleers D.,
Chintinne M.,
Denys B.,
Martens G.,
Keymeulen B.,
Gorus F.
Publication year - 2008
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/j.1463-1326.2008.00941.x
Subject(s) - type 2 diabetes , diabetes mellitus , cell , mass cytometry , medicine , population , disease , cell type , islet cell transplantation , phenotype , bioinformatics , islet , immunology , endocrinology , biology , biochemistry , environmental health , gene
Type 1 and type 2 diabetes have often been presented as disease forms that profoundly differ in the presence and pathogenic significance of a reduced β‐cell mass. We review evidence indicating that the β‐cell mass in type 1 diabetes is usually not decreased by at least 90% at clinical onset, and remains often detectable for years after diagnosis at age above 15 years. Clinical and experimental evidence also exists for a reduced β‐cell mass in type 2 diabetes where it can be the cause for and/or the consequence of dysregulated β‐cell functions. With β‐cell mass defined as number of β‐cells, these views face the limitation of insufficient data and methods for human organs. Because β‐cells can occur under different phenotypes that vary with age and with environmental conditions, we propose to use the term functional β‐cell mass as an assessment of a β‐cell population by the number of β‐cells and their phenotype or functional state. Assays exist to measure functional β‐cell mass in isolated preparations. We selected a glucose‐clamp test to evaluate functional β‐cell mass in type 1 patients at clinical onset and in type 1 recipients following intraportal islet cell transplantation. Comparison of the data with those in non‐diabetic controls helps targeting and monitoring of therapeutic interventions.