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To the Editor: Dr Chiasson and colleagues¹ speculated that by decreasing postprandial glucose levels, acarbose could decrease oxidative stress and thus ameliorate the endothelial dysfunction associated with the postprandial state. The authors speculated that this could account for the beneficial cardiovascular effect of acarbose in patients with IGT.

However, acarbose has an additional effect that could explain these outcomes. Acarbose causes a dose-dependent increase in the amount of dietary carbohydrate entering the colon and produces a significant increase in total fecal short-chain fatty-acid content in patients with diabetes.² Short-chain fatty acids, which are produced in large amounts in the cecum and large intestine as a result of the fermentation of carbohydrates, cause vasodilation in vascular beds.^3-4 It was initially thought that the increase in short-chain fatty acids produced by acarbose did not induce an increase in their serum concentrations. However, one recent trial has found that acarbose, used at the . . . [Full Text of this Article]

José-Miguel González-Clemente, MD, PhD; Emilio Ortega-Martínez de Victoria, MD; Olga Giménez-Palop, MD; Dídac Mauricio, MD, PhD
Department of Diabetes, Endocrinology and Nutrition
Hospital de Sabadell
Sabadell, Spain

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