Concerning the lipid levels, the significantly higher postprandial increase in the triglyceride levels and the smaller decrease in the free fatty acid levels detected in both groups after the M-meal is not surprising. Free fatty acids are known to impair insulin sensitivity and to enhance hepatic glucose production. Decreases in the levels of these components leads to improvements in insulin sensitivity and glucose tolerance based on intervention studies. We initially detected significantly lower IRI and C-peptide responses after the M-meal than the V-meal in healthy subjects. However, these levels decreasing more slowly, and after 180 min, the level of IRI was significantly higher in both groups after the Mmeal. This result indicates that after the M-meal, hyperinsulinemia persisted longer in both groups. This finding is in accordance with a glucose clamp study of nondiabetic human subjects indicating that increases in the FFA levels lead to insulin resistance within several hours. Several studies confirmed that meals containing higher protein and/or fat contents exert an additional impact on the postprandial insulin Euphorbia-factor-L1 demand and the increase in the glucose levels. In patients suffering from type 1 diabetes, high-fat meals containing identical carbohydrate and protein contents Genkwanin required a larger dose of insulin than low-fat meals. Furthermore, addition of protein increases the insulin demand. Carbohydrate, fat and protein in the lumen of the gut have been demonstrated to stimulate the secretion of a broad range of GIHs. The incretin effect, the postprandial augmentation of insulin secretion by gut hormones, has been primarily associated with the secretion and insulinotropic effect of two GIHs �C GIP and GLP-1. The incretin effect is thought to mediate approximately 50�C70% of the overall insulin response after a mixed meal or glucose ingestion in healthy subjects. It is well understood that in patients with diabetes, the incretin effect is diminished secondarily, and this result appears to be due to impaired beta cell sensitivity.