The blockade of GIP action appears promising as a new and potentially important approach to treat obesity-related diabetes. PYY is released postprandially from gastrointestinal L-cells with GLP-1 and oxyntomodulin and has anorexic effects. In healthy humans stimulation of PYY and PP is dependent on fat digestion. In obese subjects, the altered postprandial secretion of PYY is a Ergosterol consequence of a dysfunction of L cells, which become less sensitive to the positive feedback effect of lipids. The positive correlation of changes in amylin, insulin and Cpeptide observed by the authors is not surprising. Amylin is a peptide co-secreted with insulin. The role of amylin in the pathogenesis of T2D has been suggested by in vitro and in vivo studies indicating its effect to cause insulin resistance and/or inhibit insulin secretion. It is worth noting that amylin interacts with numerous other gastrointestinal hormones to control eating and mediate the eating inhibitory effect of some of these hormones, most prominently peptide YY and GLP-1. These combinations lead to a stronger reduction of eating control than single hormones alone. Thus the diminished effect of amylin is possibly important for other gastrointestinal hormones.The positive correlation between postprandial changes in amylin and triglycerides is in accordance with a study which demonstrated a strong association of amylin with inflammatory markers and metabolic syndrome including triglycerides in healthy individuals. On the other hand, postprandial changes in PP associated negatively with triglycerides changes and positively with FFA changes in patients with T2D. As suggested earlier, elevated plasma PP may be viewed as a negative marker and it has been demonstrated that after diet-induced weight loss, the decrease in PP correlated negatively with improvement in b-cell function. To the best knowledge of the authors, the association between PP and postprandial (R)-(-)-Modafinic acid lipids has not been published yet. We observed lower fasting and postprandial plasma ghrelin and diminished postprandial suppression of ghrelin secretion in patients with T2D. That is in accordance with the previously demonstrated lower concentrations of ghrelin in response to weight gain, overfeeding and a high-fat diet. Metformin prolongs the postprandial fall in ghrelin concentrations in patients with 
T2D, which is one of its potential mechanisms of promoting weight loss. A negative association was found between postprandial changes in ghrelin and in triglycerides. Although the authors of this study are the first ones to demonstrate a direct association between these variables, there is already some evidence in the literature supporting their finding: It has been demonstrated that a highfructose diet attenuates postprandial suppression of ghrelin and increases triglycerides in healthy women, however the association has not been tested by the authors. One experimental study demonstrated that ghrelin administration lowers muscle triglycerides in rat muscle. As a new finding the authors observed a positive relationship of postprandial changes in GIP and PYY with changes in ascorbic acid in patients with T2D. The correlation does not prove any causal relationship. Either the primary defect is the dysfunction of L and K cells of the intestine, resulting in abnormalities in postprandial plasma glucose and lipids and causing an increased oxidative stress, or the primary defect is the increased postprandial oxidative stress due to hyperglycemia and hyperlipidemia, causing a dysfunction of L and K cells.