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The factors that normally regulate the proliferation of the insulin-producing pancreatic [beta]-cell largely remain elusive although several factors have been identified that influence [beta]-cell growth in vitro. The adult [beta]-cell is normally virtually quiescent, but its replicatory activity can be enhanced in vitro by certain nutrients and growth factors, and long-term alterations in [beta]-cell mass constitute an important means to accommodate an increased demand for insulin. Likewise, expansion of the [beta]-cell mass by recruitment of [beta]-cells to proliferate may constitute a means by which the organism can compensate for the loss or dysfunction of [beta]-cells occurring in diabetes. However, neither in human or animal models for type-1 diabetes, nor in type-2 diabetes, is [beta]-cell regeneration a noteworthy feature. Thus, if [beta]-cells could be induced to replicate at a higher rate, this may prove beneficial in maintaining normoglycaemia, since the [beta]-cell mass is a major determinant of the total amount of insulin that can be secreted by the pancreas. The present review will focus on the normal regulation of [beta]-cell mitogenesis and hormones production in vitro and in vivo, and furthermore, will present evidence for an insufficient extent of [beta]-cell regeneration in different forms of diabetes mellitus. Additionally, the possibility of manipulating [beta]-cell proliferation by peptides and genetic engineering, and the significance of [beta]-cell mitogenesis in islet transplantation will be discussed in relation to treatments of diabetes mellitus.

(C) 1996 Blackwell Science Ltd.