The interactions of glucose metabolism and biological rhythms in mammals mark the framework of this thesis. The influence of melatonin on the insulin-secreting pancratic β-cell was of particular interest. Previous studies demonstrated an insulin-inhibiting influence of melatonin, mediated by cAMP. However, the inositol-1,4,5-trisphosphate (IP3) pathway is involved in the insulin secretory response as well, and the melatonin signal may play a part in its regulation. To adress this question, INS1 rat insulinoma cells served as a model for pancreatic β-cells. Cells were stimulated in batch culture and in a dynamic superfusional system. Insulin and intracellular IP3-levels were measured. An IP3-radioreceptorassay was established and adopted to this type of cells. These experiments were supported by molecularbiological studies focusing on IP3-receptors. In conclusion, there is a specific dose-dependant stimulation of IP3 in pancreatic β-cells by melatonin. However, the cAMP- and subsequently insulin-inhibiting signaling pathway is predominant in terms of insulin release. Obviously, the melatonin in the pancreatic β-cells is coupled to parallel signaling pathways, with contradictory influences on insulin secretion.