R. Rabasa-lhoret et al., Use of an alpha-glucosidase inhibitor to maintain glucose homoeostasis during postprandial exercise in intensively treated Type 1 diabetic subjects, DIABET MED, 18(9), 2001, pp. 739-744
Aim We evaluated the effects of an alpha -glucosidase inhibitor, acarbose,
on glucose homoeostasis during postprandial exercise in Type 1 diabetic sub
jects.
Methods Seven Type 1 diabetic subjects with good glycaemic control on ultra
lente-regular insulin were randomized in a single blind cross-over study to
acarbose 100 mg or placebo taken with a mixed meal (600 kcal, 75 g carbohy
drates), followed 90 min later by 30 min of exercise at 50% maximum aerobic
capacity. Glucose turnover was measured by tracer (d-[6,6,H-2(2)]glucose)
methodology, and intestinal glucose absorption was quantified using carbohy
drate polymers labelled with [C-13]glucose.
Results Acarbose resulted in a significant decrease in the postprandial gly
caemic rise (mean +/- SEM 2.9 +/- 0.6 vs. 5.0 +/- 0.7 mmol/l; P < 0.005) an
d in the glycaemic nadir during exercise (- 0.8 +/- 0.6 vs. 0.9 +/- 1.3 mmo
l/l below baseline; P < 0.05). Total glucose appearance increased similarly
under the two treatments during the postprandial (27.0 vs. 27.9 mu mol per
kg per min) and exercise (33.9 vs. 33.5 mu mol per kg per min) periods. Me
an glucose absorption was significantly delayed by acarbose (7.8 vs. 10.2 m
u mol per kg per min; P < 0.02), but was compensated by the lack of postpra
ndial suppression of hepatic glucose production (106% of basal hepatic gluc
ose production vs. 81%; P < 0.006). Episodes of hypoglycaemia were no diffe
rent (three vs. six).
Conclusion These results indicate that, in Type 1 diabetic subjects, acarbo
se results in a better glycaemic profile during postprandial exercise and s
uggest that it could lead to a lower risk of exercise-induced hypoglycaemia
due to delayed glucose absorption and less suppression of hepatic glucose
production.