Affiliation:
1. Department of Genetic Medicine and Development, University of Geneva Medical School, 1 rue Michel-Servet, CH-1211 Geneva 4, Switzerland
Abstract
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.
Cited by
14 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献