Effect of Acarbose on the Hormonal and Metabolic Response to the Simultaneous Ingestion of Sucrose and Ethanol
Previous studies have demonstrated that ethanol potentiates the insulin response to sucrose ingestion and favors the occurrence of reactive hypoglycemia. The present study aimed at investigating the effects of acarbose, an α-glucosidase inhibitor, on the hormonal and metabolic response to sucrose and ethanol. Six healthy male volunteers (26.5 ± 0.8 years of age; 104.4 ± 5.4% of IBW) ingested a 600-ml mixture of 75 g sucrose and 50 g ethanol dissolved in water. A dose of 100 mg acarbose (ACAR) or a placebo (PBO) was ingested at time 0, in a randomized protocol. Parameters investigated included blood glucose (BG), ethanol (ALC), fructose, plasma insulin (IRI), glucagon (IRG), and rates of appearance (Ra) and disappearance (Rd) of glucose, using 3-[3H]glucose. After PBO, the simultaneous ingestion of sucrose and ALC induced a 70 mg/dl rise in BG followed by a moderate reactive hypoglycemia (BG nadir, 56.5 ± 4.2 mg/dl), a 5 mg/dl rise in blood fructose, a marked rise in IRI (100 μU/ml at the 60th min), and a moderate fall in IRG. After ACAR, the BG rise was significantly (2p < 0.01) inhibited (+ 27 mg/dl at the 60th min), the blood fructose response was negligible, the plasma IRI response was markedly reduced, and the plasma IRG inhibition was more pronounced. The BG nadir was 64.5 ± 3.5 mg/dl and occurred about 1 h later. The hypoglycemic index of Cole et al.  was significantly reduced by ACAR: 0.21 ± 0.05 versus 0.98 ± 0.23 (2p < 0.05). Both Ra and Rd were markedly reduced after ACAR. Blood ethanol peak was similar after ACAR (0.82 ± 0.08 g/l) and PBO (0.77 ± 0.14 g/l), but it occurred some 45 min later after ACAR. Moreover, the rate of fall of blood ALC was significantly (2 p < 0.025) lower after ACAR (9.2 ± 1.3 mg/dl per hour) than after PBO (15.4 ± 2.4 mg/dl per hour).