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Effect of lowering postprandial hyperglycemia on insulin secretion in older people with impaired glucose tolerance

¹Department of Internal Medicine, University of Michigan, Ann Arbor 49109; and ²Institute of Gerontology, University of Michigan, Ann Arbor, Michigan 48109

Submitted 2 April 2004 ; accepted in final form 18 June 2004

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 yr) with IGT treated with the -glucosidase inhibitor acarbose (n = 14) or placebo (n = 13) for 6 wk in a randomized, double-blind study. Baseline and posttreatment studies included 1) an oral glucose tolerance test (OGTT), 2) 1-h postprandial glucose monitoring, 3) a frequently sampled intravenous glucose tolerance test (insulin sensitivity, or S_I), and 4) glucose ramp clamp (insulin secretion rates, or ISR), in which a variable glucose infusion increases plasma glucose from 5 to 10 mM. The treatment groups had similar baseline body mass index; fasting, 2-h OGTT, and 1-h postprandial glucose levels; and 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-h postprandial glucose levels (6.9 ± 0.3 vs. 8.2 ± 0.4 mM, P = 0.02) were significantly lower in the acarbose than in the placebo group. Despite this reduction of chronic hyperglycemia in the acarbose vs. placebo group, 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.

-cell function; glucose intolerance; aged humans

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