Glucose homeostasis is tightly controlled by, first and foremost, insulin. There is a minute-to-minute regulation of insulin output from the Beta cell to meet changing demands at and between meals. There is also a long-term adaptation of insulin production by changes in total Betacell mass. Diabetes mellitus develops if any one of these processes is insufficient and causes absolute or relative insulin deficiency. The regulation of insulin biosynthesis and release in relation to the aetiology of diabetes has been intensely studied, while the role of Beta-cell growth has met with less interest until recent years. In Type 1 (insulin-dependent) diabetes there is a loss of Beta cells and decompensation of metabolism following autoimmune aggression [1]. Insulin production often reccurs shortly after onset of clinical disease (" honeymoon period") suggesting an effort by the reduced Beta-cell mass to meet insulin demands. In Type 2 (non-insulin-dependent) diabetes pathogenesis is less clear and probably multifactorial but there is evidence to suggest that a reduced insulin secretory response to glucose and a limited capacity for Beta-cell replication predisposes to the disease [2, 3]. Studies of the regulation and limitations of Beta-cell growth thus appear appropriate for the understanding of the aetiology and pathogenesis of diabetes. Present knowledge on the regulation of Beta-cell growth, with emphasis on recent studies of Beta-cell DNA replication in vitro, is reviewed in this paper.