There is a growing body of evidence that postprandial hyperglycaemia plays an important role in accelerated atherosclerosis and may be a therapeutic target for preventing cardiovascular disease (CVD) in diabetes. However, there is no convenient biomarker that could reflect cumulative postprandial hyperglycaemia in diabetes. We have recently found that glyceraldehyde can rapidly react with amino groups of proteins to form glyceraldehyde-derived advanced glycation end products (AGEs), which evoke vascular inflammation and endothelial dysfunction, thereby being implicated in accelerated atherosclerosis in diabetes. In this study, we examined whether glyceraldehyde-derived AGEs were a biomarker that could reflect cumulative postprandial hyperglycaemia in Goto-Kakizaki (GK) rats fed twice a day. GK rats at 8 weeks of age were divided into 2 groups; either the vehicle (VEH) or 50 mg/kg of nateglinide (NAT) was administered twice daily just before each meal. After 6 weeks, nateglinide treatment was found to not only prevent postprandial hyperglycaemia, but also reduce glyceraldehyde-derived AGE levels in GK rats fed twice a day. However, there was no significant difference in HbA1c or glucose-derived AGE levels between the two groups. The present study demonstrated for the first time that glyceraldehyde-derived AGEs, but not HbA1c or glucose-derived AGEs, were a biomarker that could reflect cumulative postprandial hyperglycaemia in diabetic rats. Glyceraldehydederived AGEs may be a novel therapeutic target for preventing CVD in diabetes.