A study of the effect of oral glucose loading on plasma oxidant:antioxidant balance in normal subjects

Summary

Background

Antioxidant defence has been reported to decrease, and oxidative stress to increase, after oral glucose loading in both normal and diabetic subjects. If confirmed in normal subjects, glucose–induced antioxidant depletion has important implications for health in relation to the modern, sugar–rich diet.

Aim of the study

To investigate changes in plasma biomarkers of oxidant:antioxidant balance in non–diabetic subjects following oral glucose loading. Baseline inter–relationships between biomarkers of glycaemic control, oxidant:antioxidant balance and inflammation were also explored.

Methods

A singleblinded, placebo–controlled, crossover intervention trial involving 10 healthy, consenting subjects. Venous blood was collected after ingestion of 75 g glucose in 300 mL water, or of water alone. Blood was collected at 0 time (fasting) and 30, 60, 90, 120 min post–ingestion. Within 2 weeks the procedure was repeated with volunteers crossedover onto the other treatment. Plasma total antioxidant capacity (as the FRAP value), ascorbic acid, α–tocopherol, uric acid, malondialdehyde (MDA), allantoin and high sensitivity C–reactive protein (hsCRP), glucose and insulin, were measured in all samples. Paired results post–glucose and post–water at each time interval were compared using the Wilcoxon matched–pairs signed–ranks test.

Results

Normal glucose tolerance was observed in all subjects, although, as expected, plasma glucose and insulin increased significantly (p < 0.05, n = 10) after glucose loading. Post–glucose responses in plasma FRAP and the individual antioxidants tested were not significantly different to the responses seen post–water, although both FRAP and α–tocopherol decreased slightly. Neither were postglucose changes in plasma MDA and allantoin, putative biomarkers of oxidative stress, significantly different to those after intake of water alone. Plasma FRAP and α-tocopherol also decreased slightly, but not significantly, after intake of water. A significant direct correlation (r = 0.867, p < 0.001, n = 10) was found between fasting allantoin and (log transformed) hsCRP concentrations.

Conclusions

These new data from a controlled intervention trial indicate that acute, transient increases in plasma glucose following oral intake of a large glucose load do not, as previously reported, cause a significant decrease in plasma antioxidants or increase oxidative stress in non–diabetic subjects. This is reassuring given the large quantities of sugar ingested by children and adolescents. However, a small decrease in plasma antioxidant capacity was seen after ingestion of water and of glucose, and it is possible that intake of glucose without concomitant intake of antioxidants in susceptible individuals may cause oxidative stress. Further work is needed in relation to diabetic subjects and a possible glucose threshold for this. The finding of a direct relationship between allantoin, a biomarker of oxidative stress, and hsCRP, a marker of inflammation and CHD predictor, in healthy subjects is interesting and indicates a link between sub–clinical inflammation and oxidative stress.