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The pancreas is constituted by two distinctly different tissues: the exocrine component, i.e., pancreatic acinar cells that secrete digestive enzymes; and the endocrine component, the islets of Langerhans, constituted by hormone secreting cells. In the islet, the ┙-cells produce glucagon; the ┚-cells, insulin; the ├-cells, somatostatin; ┛-cells, pancreatic polypeptide (Figure 1). Diabetes is caused either by an absolute (type 1) or relative (type 2) defect of insulin-producing ┚-cells in the pancreas. Therefore, regardless of the different pathogenesis, diabetes is the perfect candidate for cell replacement therapy. Currently the two available alternatives for ┚-cell replacement therapy are whole pancreas or isolated islet transplantation (Shapiro et al., 2000). However, these approaches are severely limited by a shortage of human organ donors and the need of lifelong immunosuppressive therapy. In the absence of other clearly suitable and renewable sources of surrogate ┚-cells, an alternative strategy to exogenous cell replacement therapy might be fostering endogenous ┚-cell regeneration. Therefore, knowledge of the mechanisms regulating ┚-cell plasticity in both embryonic and adult life, as well as in pathological conditions, is of particular interest. During pancreatic development, ┚-cells derive from a population of endocrine precursors arising from the pancreatic epithelium (Gittes, 2009). Activation of cell-specific transcription factors guides the initially multipotent progenitors and determines their differentiation into mature ┚-cells. The final size of the endocrine pancreas is limited by the size of the progenitor cell pool in the developing pancreatic bud (Stanger et al., 2007). After birth, most ┚-cells are considered quiescent, however, it has been shown that the ┚-cell mass can adaptively expand under some physiologic or pathologic circumstances, such as pregnancy and obesity, both in mammals and rodents (Bernard-Kargar & Ktorza, 2001). In mouse models there is also evidence that the pancreas preserves the ability to regenerate its ┚-cell mass in response to several non-physiological injuries, such as selective chemical destruction or surgical excision (Trucco, 2005; Thorel, 2010). Furthermore, in non-obese diabetic mice (NOD) it has been shown that recovery of sufficient endogenous insulin

The Enigma of &#946;-Cell Regeneration in the Adult Pancreas: Self-Renewal Versus Neogenesis

The Enigma of β-Cell Regeneration in the Adult Pancreas: Self-Renewal Versus Neogenesis