In the course of pregnancy increasing insulin resistance develops due to deteriorated phosphorylation of the insulin receptor and its substrate (IRS-1). As a result of relations between secretion and the action of insulin the beta-cell reacts by insulin hypersecretion and thus the development of hyperinsulinaemia is influenced. Furthermore pregnancy is characterized by increasing differences between the anabolic and catabolic stage in the intermediary metabolism manifested in particular by a tendency towards ketosis and hypoglycaemia during fasting and also by hypoaminoacidaemia. In addition to these metabolic changes there are also other laboratory deviations, manifested e.g. by hyperfibrinogenaemia and an increased concentration of tPA inhibitor (PAI-1) without detectable endothelial dysfunction. The increasing albuminuria is not a manifestation of developing nephropathy but the sign of functional changes which after delivery disappear very quickly. The mentioned deviations are the consequence of altered hormonal regulations in the course of pregnancy, while after delivery the baseline state present before pregnancy is restored.

        Key words: Pregnancy - Insulin resistance - Hyperinsulinaemia - Ketone bodies - Hypoaminoacidaemia - Albuminuria