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Evidence of ?-Cell Dedifferentiation in Human Type 2 Diabetes #MMPMID26713822
Cinti F; Bouchi R; Kim-Muller JY; Ohmura Y; Sandoval PR; Masini M; Marselli L; Suleiman M; Ratner LE; Marchetti P; Accili D
J Clin Endocrinol Metab 2016[Mar]; 101 (3): 1044-54 PMID26713822show ga
Context:: Diabetes is associated with a deficit of insulin-producing ?-cells. Animal studies show that ?-cells become dedifferentiated in diabetes, reverting to a progenitor-like stage, and partly converting to other endocrine cell types. Objective:: To determine whether similar processes occur in human type 2 diabetes, we surveyed pancreatic islets from 15 diabetic and 15 nondiabetic organ donors. Design:: We scored dedifferentiation using markers of endocrine lineage, ?-cell-specific transcription factors, and a newly identified endocrine progenitor cell marker, aldehyde dehydrogenase 1A3. Results:: By these criteria, dedifferentiated cells accounted for 31.9% of ?-cells in type 2 diabetics vs 8.7% in controls, and for 16.8% vs 6.5% of all endocrine cells (P < .001). The number of aldehyde dehydrogenase 1A3-positive/hormone-negative cells was 3-fold higher in diabetics compared with controls. Moreover, ?-cell-specific transcription factors were ectopically found in glucagon- and somatostatin-producing cells of diabetic subjects. Conclusions:: The data support the view that pancreatic ?-cells become dedifferentiated and convert to ?- and ?-?like? cells in human type 2 diabetes. The findings should prompt a reassessment of goals in the prevention and treatment of ?-cell dysfunction.