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  • Title: Effects of 8-wk alpha-glucosidase inhibition on metabolic control, C-peptide secretion, hepatic glucose output, and peripheral insulin sensitivity in poorly controlled type II diabetic patients.
    Author: Schnack C, Prager RJ, Winkler J, Klauser RM, Schneider BG, Schernthaner G.
    Journal: Diabetes Care; 1989 Sep; 12(8):537-43. PubMed ID: 2673693.
    Abstract:
    Miglitol (BAYm 1099), an alpha-glucosidase inhibitor, reduces the postprandial increase of blood glucose and serum insulin levels in type II (non-insulin-dependent) diabetes mellitus, as shown in short-term studies. In this study, the effects of long-term miglitol treatment on metabolic control, C-peptide secretion, hepatic glucose output, and peripheral insulin sensitivity (euglycemic clamp) were tested in 15 type II diabetic patients (8 receiving insulin, 7 receiving oral hypoglycemic agents). For 8 wk they received either miglitol (300 mg/day) or placebo with a double-blind crossover design that had a 4-wk washout period between treatments. Miglitol therapy induced a reduction of postprandial blood glucose levels (miglitol compared with placebo; areas under the curve; P less than .002), whereas fasting blood glucose levels were not influenced. Miglitol caused a slight reduction of glycosylated hemoglobin levels (mean +/- SE miglitol and placebo 9.50 +/- 0.3 and 10.0 +/- 0.4%, respectively; P less than .05), which was more pronounced in insulin-treated patients. Miglitol caused a reduction of postprandial C-peptide increase (P less than .03). Hepatic glucose output (both in the basal state and during euglycemic clamp conditions) and peripheral insulin sensitivity were not influenced by miglitol therapy. Specific side effects were observed in 11 patients; in 6 patients only to a moderate degree. Long-term miglitol treatment induces a persistent reduction of postprandial blood glucose increase. This effect is more pronounced in type II diabetic patients on insulin therapy, which can cause a moderate improvement of overall metabolic control.
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