Glucose tolerance declines with age, resulting in a high prevalence of diabetes and impaired glucose tolerance (IGT) in the older population. Hyperglycemia per se can lead to impaired - cell function (glucose toxicity). We tested the role of glucose toxicity in age-related -cell dysfunction in older people (65 ± 8 years) with IGT treated with the -glucosidase inhibitor, acarbose (n=14), or placebo (n=13) for 6 weeks in a randomized, double-blind study. Baseline and post-treatment studies included: 1) oral glucose tolerance test (OGTT), 2) 1-hour postprandial glucose monitoring, 3) frequently sampled intravenous glucose tolerance test (insulin sensitivity, S_I), and 4) glucose ramp clamp (insulin secretion rates, ISR), in which a variable glucose infusion increases plasma glucose from 5-10 mM. The treatment groups had similar baseline BMI; fasting, 2-hour OGTT, 1-hour postprandial glucose levels; or S_I. In these carefully matched older people with IGT, both fasting (5.7 ± 0.2 vs. 6.3 ± 0.2 mM, p = 0.002) and 1-hour postprandial glucose levels (6.9 ± 0.3 vs. 8.2 ± 0.4 mM, p = 0.02) were significantly lower in the acarbose vs. placebo groups. Despite this reduction of chronic hyperglycemia in the acarbose vs. placebo groups, measures of insulin secretion (ISR area under the curve: 728 ± 55 vs. 835 ± 81 pmol/kg, p = 0.9; and acute insulin response to intravenous glucose: 329 ± 67 vs. 301 ± 54 pM, p = 0.4) remained unchanged and impaired. Thus, short-term improvement of chronic hyperglycemia does not reverse -cell dysfunction in older people with IGT.