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Type 2 diabetes (T2D) is caused by an inherited predisposition to pancreatic islet β-cell failure, which is manifested under cellular stress induced by metabolic overload. The decrease in the functional β-cell mass associated with T2D has been attributed primarily to β-cell death; however, studies in recent years suggested that β-cell dedifferentiation may contribute to this decline. The mechanisms linking genetic factors and cellular stress to β-cell dedifferentiation remain largely unknown. Here I evaluate the evidence for β-cell dedifferentiation in T2D, and consider experimental systems in which its mechanisms may be studied. Understanding these mechanisms may allow prevention of β-cell dedifferentiation, or induction of cell redifferentiation for restoration of the functional β-cell mass. SIGNIFICANCE
This review evaluates the evidence for ß-cell dedifferentiation in Type 2 diabetes (T2D), and considers experimental systems in which its mechanisms may be studied. Understanding these mechanisms may allow prevention of ß-cell dedifferentiation, or induction of cell redifferentiation for restoration of the functional ß-cell mass. © AlphaMed Press 2019.
This article was published in the following journal.
Name: Stem cells (Dayton, Ohio)
Current research indicates that beta cell loss in type 2 diabetes may be attributed to beta cell dedifferentiation rather than apoptosis; however, the mechanisms by which this occurs remain poorly und...
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The reverse developmental process in which differentiated cells with specialized functions become undifferentiated PROGENITOR CELLS once again. Dedifferentiation and subsequent proliferation provide the basis for tissue regeneration and the formation of new stem cell lineages.
The time period before the development of symptomatic diabetes. For example, certain risk factors can be observed in subjects who subsequently develop INSULIN RESISTANCE as in type 2 diabetes (DIABETES MELLITUS, TYPE 2).
Autoimmune diabetes in adults with slowly progressive PANCREATIC BETA CELL failure and the presence of circulating autoantibodies to PANCREATIC ISLETS cell antigens.
A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.
A single-pass transmembrane CELL SURFACE RECEPTOR that binds ADVANCED GLYCOSYLATION END PRODUCTS to mediate cellular responses to both acute and chronic vascular inflammation in conditions such as ATHEROSCLEROSIS and DIABETES MELLITUS, TYPE 2 . It also binds AMYLOID BETA PEPTIDES and the alarmins S100A12 and S100 CALCIUM BINDING PROTEIN BETA SUBUNIT.