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Cell therapy for type 2 diabetes: is it desirable and can we get it?
Author(s) -
Halban P. A.
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.1463-1326.2008.00957.x
Subject(s) - neogenesis , beta cell , type 2 diabetes , beta (programming language) , regeneration (biology) , diabetes mellitus , adipose tissue , insulin , cell therapy , endocrinology , islet , cell , insulin resistance , inflammation , medicine , stem cell , biology , microbiology and biotechnology , computer science , genetics , programming language
The functional mass of β‐cells is decreased in type 2 diabetes. Replacing missing β‐cells or triggering their regeneration may thus allow for improved treatment of type 2 diabetes, to the extent that this is combined with therapy for improved insulin sensitivity. Although progress has been made in deriving β‐cell‐like cells from stem or precursor cells in vitro , these cannot yet be obtained in sufficient quantities or well enough differentiated to envisage their therapeutic use in β‐cell replacement therapy. Likewise, our very limited understanding of β‐cell regeneration in adult man does not yet allow for development of a valid strategy for kick‐starting such a process in individuals with type 2 diabetes, whether by bona fide neogenesis or self‐replication of existing β‐cells. Regardless of how β‐cell mass is restored in type 2 diabetes, it will be important to prevent any renewed decrease thereafter. Current understanding suggests that islet inflammation as well as signals from (insulin‐resistant/inflamed) adipose tissue and skeletal muscle contribute towards decreased β‐cell mass in type 2 diabetes. It will likely be important to protect newly formed or implanted β‐cells from these negative influences to ensure their long‐term survival.