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Cell therapy for type 2 diabetes: is it desirable and can we get it?
|Published in||Diabetes, Obesity and Metabolism. 2008, vol. 10, no. Suppl 4, p. 205-11|
|Abstract||The functional mass of beta-cells is decreased in type 2 diabetes. Replacing missing beta-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 beta-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 beta-cell replacement therapy. Likewise, our very limited understanding of beta-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 beta-cells. Regardless of how beta-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 beta-cell mass in type 2 diabetes. It will likely be important to protect newly formed or implanted beta-cells from these negative influences to ensure their long-term survival.|
|Keywords||Animals — Diabetes Mellitus, Type 2/physiopathology/therapy — Female — History, 18th Century — History, 19th Century — History, 20th Century — History, 21st Century — Humans — Insulin Resistance/physiology — Islets of Langerhans/cytology/physiology — Male — Stem Cell Transplantation/methods/trends — Tissue Therapy/methods/trends|
|Research group||Fonction de l'îlot de Langerhans (324)|