The control of glucose metabolism by pancreatic endocrine cells throughout life relies on a tight regulation of the mass of insulin-producing β-cells. How this homoeostasis is achieved is not well understood. Over the last few years, experimental rodent models with altered β-cell mass, and, more recently, new transgenic approaches designed to tackle this problem, have provided abundant information. Processes such as β-cell proliferation and apoptosis, or even β-cell differentiation from poorly characterized progenitor cells, whether immature or differentiated, appear to be implicated. A complex picture is thus emerging in which the nature of the pancreatic lesion appears to determine the kind of regenerative response. The environment formed by acinar and ductal cells, and also by vascular and neuronal structures, which surround islets and penetrate into their β-cell core, might play crucial roles so far unsuspected, which should be explored in the near future.
Conference Article| May 21 2008
Experimental models of β-cell regeneration
Pedro L. Herrera
Pedro L. Herrera 1
1Department of Genetic Medicine and Development, University of Geneva Medical School, 1 rue Michel-Servet, CH-1211 Geneva 4, Switzerland
1To whom correspondence should be addressed (email Pedro.Herrera@medecine.unige.ch).
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Claire Bonal, Isabelle Avril, Pedro L. Herrera; Experimental models of β-cell regeneration. Biochem Soc Trans 1 June 2008; 36 (3): 286–289. doi: https://doi.org/10.1042/BST0360286
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