According to recent studies, oxidative stress is supposed to be the link between acute postprandial hyperglycemia and cardiovascular risk in patients with T2D. In some studies, several markers of oxidative damage such as TBARS, isoprostanes and protein carbonyls have been found to increase 2�C 3 hours after an oral glucose load. However, there is still lack of information about the relationship of oxidative stress, gastrointestinal and appetite hormones, particularly during the postmeal phase. Evaluating the effect of gastrointestinal hormones together with changes in oxidative stress markers may contribute to better understanding of the mechanisms underlying the postprandial state in patients suffering from T2D and thus suggest new preventive and therapeutical strategies. A standard meal test was used for monitoring the postprandial concentrations of gastrointestinal hormones and oxidative stress markers in patients with T2D compared to healthy controls. To the best knowledge of the authors, they are the first ones to try to find a link between postprandial oxidative stress and gastrointestinal hormones in a clinical and physiological setting. In the study in question the authors monitored postmeal response of gastrointestinal hormones and oxidative stress markers in Ginsenoside-F5 diabetic patients and compared them with healthy controls. The postmeal phase is an important and independent predictor of macrovascular diabetic complications, more in females than in males. Postprandial hyperglycemia is a stronger cardiovascular 
risk factor in women than in men, whereas other authors state that Atractylenolide-III gender-related differences disappear after adjustment for the main cardiovascular risk factors. In our study we observed the postprandial glycemic control in the general population and the proportion of women and men was equal. Elevation of postmeal or postchallenge glucose supports the concept of “metabolic memory” which is responsible for early diabetic complications and which is closely tied to oxidative stress, namely with increased mitochondrial superoxide production. However, few studies were interested in postprandial phase after a meal test, which is more physiological as it contains all main nutrients than the usually used oral glucose tolerance test. According to Alssema study, incretin effect could be distinct after OGTT and after a standard meal test. In this study GLP-1 secretion in diabetic patients was increased following oral glucose but not after the mixed meal. Therefore, incretin secretion seems to depend on both the glucose and lipid metabolism as well. The incretin effect is diminished secondarily in T2D as a concequence of metabolic and hormonal disturbances while increased oxidative stress is directly involved in the pathogenesis of diabetes. The authors focused on clarifying whether these parameters correlated with each other and whether they had mutual influence on each other. Several studies have shown that the incretin effect is attenuated in T2D because of a severe defect in b-cell sensitivity to GIP, which has an insulinotropic effect. It has also been suggested that changes in insulin secretion following a lifestyle intervention might be mediated via alterations in GIP secretion. GIP, secreted strongly in response to fat ingestion, is involved in the translation of excessive amounts of dietary fat into adipocyte tissue stores. Patients with T2D are resistant to the biological effects of GIP. Specific GIP receptor antagonists improve glucose tolerance and b-cell function by amelioration of insulin resistance in ob/ob mice.