To examine the clinical role of BAYm 1099, 15 diettreatednon-insulin-dependent diabetic (NIDDM) subjects were randomized to start drug (50 mg 3 times/ day) or placebo after a 4-wk run-in period in a doubleblind crossover study. Treatment periods (4 wk) were separated by a 2-wk washout period. During the last week of each treatment period, three test meals (TMs) were administered: 60 g starch (TM1), 25 g sucrose (TM2), and combined 60 g starch and 25 g sucrose (TM3). Twelve subjects completed the study. The peak postprandial blood glucose, lactate, and pyruvate levels (means ± SE) were significantly lower with active drug after all test meals, particularly TM2 (11.3 ±1.0 vs. 14.3 ± 1.4 mM, P <.001; 1.53 ± 0.20 vs. 2.48 ± 0.17 mM, P < .001; and 105.1 ± 17.6 vs. 147.6 ± 11.1 μM, P < .05, respectively. Peak blood glucose levels were significantly delayed. However, fasting blood glucose, HbA1, fructosamine, and cholesterol did not change during active treatment (10.0 ±1.0 vs. 9.9 ±1.0 mM, 10.0 ± 0.7 vs. 9.4 ± 0.7%, 2.44 ± 0.10 vs. 2.37 ± 0.07 mmol/100 g protein, and 6.7 ± 0.3 vs. 6.5 ± 0.3 mM, P NS). Flatulence and diarrhea were severe in 2 subjects, requiring termination of study. Thus, in NIDDM, BAYm 1099 was effective in diminishing and delaying postprandial excursions of blood glucose, lactate, and pyruvate after high- and low-sucrose meals, but overall metabolic control remained unchanged. The results of acute studies on food absorption cannot be extrapolated to predict longer-term effects on glycemic control in diet-treated NIDDM subjects.

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