Psychostimulants, such as amphetamine (AMP), methamphetamine (METH) and cocaine (COC) have been shown to cause transient disruptions of serotonin- (5-HT), dopamine- and norepinephrine signaling, as well as permanent alterations in physiology of children, that were prenatally exposed to these substances. However, there is nearly nothing known about the effects of prenatal psychostimulant exposure on glucose homeostasis. Here we show, that prenatal exposure to psychostimulants results in decreased insulin expression in pancreatic β-cells, which in turn causes a diabetic onset in mice. Using immunohistochemistry, we give evidence, that psychostimulant exposure not only permanently alters expression of serotonin synthesizing enzyme tryptophan hydroxylase 2, but also results in decreased 5-HT levels in β-cells. Similarly, we show, that levels of 5-HT receptors 1a and 2b are not affected by prenatal exposure to AMP, METH, or COC. Finally, our data links decreased insulin- and 5-HT- contents of β-cells to downregulation of transcription factor Fev, that shows a decrease in mRNA levels upon prenatal exposure to psychostimulants. Overall, this thesis gives evidence, that prenatal exposure to AMP, METH and COC, disrupts insulin- and 5-HT- pathway in the endocrine pancreas of mice.