Knowledge of pancreatic cells and their proliferation has proved to be essential to better understanding of the pathogenesis, clinical course, and prognosis of pancreatic diseases. Studies had been conducted by means of in vivo autoradiography into pancreatic cell proliferation in normal rats of various age groups (Laucke and Müller 1988; Müller et al. 1990). Described in this paper are investigations by means of in vivo autoradiography, using tritium-thymidine, which were conducted with a view to clearing up proliferation of pancreatic cells in rat under conditions of alloxan-induced diabetes. Labelling of the acinar, islet, and duct cells were found to undergo initial elevation, after two days of alloxan-induced diabetes. Labelling indices rose by three to four times, as compared to those recordable from normal rats (Laucke und Müller 1988; Müller et al. 1990). Labelling indices of acinar and islet cells went down along with the length of diabetes and, subsequently, stayed nearly constant at a level of less than one thousandth, on the 14th and 28th experimental days. Labelling of duct cells decreased the same way up to the 14th day of the experiment, though increase was recordable, especially from the small pancreatic ducts, on the 28th day. Initial elevation of labelling indices of acinar, islet, and duct cells was followed by "exhaustion". Experimental findings appeared to suggest physiological regeneration of islet cells and their replacement after injury in the adult pancreas to originate from small pancreatic ducts by "ductular proliferation". This conclusion seemed to be supported by the increase on the 28th day of the experiment of the labelling index of pancreatic duct cells, as described in this paper.(ABSTRACT TRUNCATED AT 250 WORDS)