Introduction: Due to an insulinotropic and cytoprotective influence on pancreatic β cells of incretins (glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), their agonists and inhibitors of their degradation enzyme (DPP-4) are nowadays a new therapeutic tool in the treatment of DMt2 and obesity. Under the influence of nutritive stimuli, incretins are produced and released first of all from K and L cells of the small intestine.Genome-wide association studies (GWAS) have shown only few chromosome regions significantly connected to DMt2 in men. Examples of these are genes TCF7L2 PPARγ.The Aim of the study was to compare the influence of lipids and glycaemia on fasting and postprandial incretin release in healthycontrols and patients with metabolic syndrome MS), especially in carriers of selected alleles of genes responsible for higher concentrations of FFA in blood.Patients and Methods: The investigation group (MS) consisted of 50 patients with MS (IDF 2005), but not diabetes mellitus. The control group (C) consisted of 18 healthy volunteers. Participants underwent a 3-hour OGTT and an 8-hour OLTT. During both tests blood concentration of glucose, insulin, incretins and FFA was measured. For genetic measurements the RFLP method was used. Presence of polymorphisms in the genes TCF7L2 (rs7903146) and PPARγ2 (rs1801282) were investigated.Results: Fasting and during both tests incretin concentration did not differ between MS and C groups without considering the genotype. The relation between the incretins and MS markers concentration was confirmed. In the whole group, in the fasting state, GLP-1 secretion positively correlated with carbohydrates, while FFA level correlated with GIP.It was found out that carbohydrates have a higher influence on postprandial GIP output than lipids in patients with MS, carriers of allele T of the TCF7L2 gene. This suggests that the dietary recommendation for these patients should stress the carbohydrate-based diet which seems to stimulate GIP with its protective activity output in these T allele carriers.The higher stimulation of GLP-1 by lipids in the postprandial state in patients with MS and the CC polymorphism of TCF7L2 was observed.Conclusions: The above results suggest the possibility of establishing rules of individual dietary recommendations in the prevention and treatment of pancreatic β cells damage in patients with MS, especially in carriers of different alleles of the examined polymorphism of TCF7L2. Diet selection should be based on the results of functional tests (OGTT and OLTT) performed with a parallel measurement of concentrations of GLP-1 and GIP.