Growth factors act after specific binding with cell membrane receptors, i.e. these factors mediate mitogenic signals. Insulin-like growth factors (IGF) (syn.: somatomedins) as well as insulin have the same biological activity caused by structural homology. But under normal physiological conditions neither IGF I nor IGF II appear to be involved in the regulation of glucose homeostasis, in contrary to insulin IGFs have mostly mitogenic features. On the other side it is possible that under pathophysiological conditions hypoglycemic effects are caused by an increase of free IGF in the circulation. Insulin acts as a regulating factor in the GF-expression. IGF-I and IGF-II are different peptides especially regarding to their biological role. The synthesis of IGF-I secretion in the liver is dependent on growth hormone (GH). GH is secreted by the pituitary under the influence of the growth-hormone releasing factor (GHF) and is inhibited by somatostatin. In response to GH the liver secretes somatomedin which exerts negative feed back effects on the pituitary and stimulates somatostatin release. The IGF-synthesis is dependent on the human placental lactogen (HPL), i.e. IGF-II is mainly responsible for fetal development the estimation of the production of IGFs by the fetus supports investigations about fetal somatomedins to clear fetal growth retardations and diabetic macrosomia respectively.