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Readers of Dagogo-Jack and Santiago's¹ excellent review of type 2 diabetes may be unaware that the embers of controversy regarding the effects of sulfonylureas on the heart in patients with type 2 diabetes, originally raised by the much maligned University Group Diabetes Program study,² have been fanned by a series of basic science and animal experiments conducted over the past decade.³

Briefly, sulfonylureas bind to specific membrane receptors on the beta cell causing membrane depolarization by closing the adenosine triphosphate–dependent potassium channel (K_ATP),⁴ thereby permitting an increase in intracellular calcium that leads to insulin secretion. The sulfonylurea receptor is a member of the adenosine triphosphate–binding family of receptors, and similar receptors are in the heart.⁵ Acute myocardial ischemia results in opening of K_ATPchannels with a reduction in calcium influx and a resultant decrease in myocardial contractility, which may protect the heart by reducing oxygen demand.⁶ Furthermore, brief ischemic . . . [Full Text of this Article]

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