Abstract
Background/aims. Postprandial hyperglycemia, an independent risk factor for cardiovascular disease, is accompanied by endothelial dysfunction. We studied the effect of oral glucose load on insulin and glucose fluctuations, and on postprandial endothelial function in healthy individuals in order to better understand and cope with the postprandial state in insulin resistant individuals. Methods. We assessed post-oral glucose load endothelial function (flow mediated dilation), plasma insulin, and blood glucose in 9 healthy subjects. Results. The largest increases in delta FMD values (fasting FMD value subtracted from postprandial FMD value) occurred at 3 hours after both glucose or placebo load, respectively: 4.80 ± 1.41 (P = .009) and 2.34 ± 1.47 (P = .15). Glucose and insulin concentrations achieved maximum peaks at one hour post-glucose load. Conclusion. Oral glucose load does not induce endothelial dysfunction in healthy individuals with mean insulin and glucose values of 5.6 mmol/L and 27.2 mmol/L, respectively, 2 hours after glucose load.
Highlights
Postprandial hyperglycemia is an independent risk factor for cardiovascular disease (CVD) in insulin-resistant individuals with type 2 diabetes or with the prediabetic state, impaired glucose tolerance (IGT) [1,2,3,4,5,6,7,8,9,10]
Delta flow mediated dilation (FMD) values ± SEM for post-glucose load and postplacebo load showed increasing FMD delta values for both days
The largest post-glucose load increase occurred at 3hPG (P = .009); compared to baseline, the increase was already significant at 1hPG (P = 0.03)
Summary
Postprandial hyperglycemia is an independent risk factor for cardiovascular disease (CVD) in insulin-resistant individuals with type 2 diabetes or with the prediabetic state, impaired glucose tolerance (IGT) [1,2,3,4,5,6,7,8,9,10] In line with these epidemiologic data, several studies have shown impairment of endothelial function, one of the earliest markers of atherosclerosis [11] after a meal or glucose challenge, in individuals with diabetes or IGT [12,13,14,15,16,17]. These seemingly conflicting results could be attributed to differences in methodology and subject characteristics: diverging periods of post-glucose load observations, varying periods of exposition to different concentrations of glucose, diverging criteria in subject selection, enabling versus blocking insulin’s physiologic response, and administrating oral glucose load versus intra-arterial or intravenous glucose administration
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
