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Unlike Kir6.2, Kir6.1 transfection with HEK 293 cells alone displayed the channel activity.However, when co-transfected with SUR, Kir6.1 obtained sensitivity to ATP and sulfonylurea [32, 33].Since the p conductance expressed in a NIH3T3 cell permanently transfected with a Kir6.1 clone.

A schematic representation of the mechanism of insulin secretion from pancreatic the β-cell.

The glucose transporter (GLUT2) in the β-cell membrane works so efficiently that cytoplasmic glucose can attain a high enough level to be used as the principal fuel for mitochondrial ATP production. The putative protein structure shows 13 transmembrane segments and two ATP-binding sites, indicating that it is a member of the ATP-binding cassette (ABC) transporter superfamily.

During antimalarial treatment with quinine, an optical isomer of quinidine (prototype of Vaughan Williams class Ia antiarrhythmics), severe hypoglycemic attacks have been reported [9, 10].

Quinine has been shown to block pancreatic ATP-sensitive K) channels [11, 12].

According to the clinical literature [1–8], antiarrhythmic-drug-induced hypoglycemia appears to be associated with hypoalbuminemia, renal insufficiency or diabetes mellitus, especially in elderly patients.

Therefore, special care should be paid to elderly diabetic patients who are already receiving sulfonylureas because renal dysfunction is one of the most common complications in this cohort of patients.

In rat β-cells, ADP (100 μM) was found to recover cibenzoline (10 μM)-, but not glibenclamide (1 μM)-induced block of channel activity [16].

These experimental results suggest that antiarrhythmic agents bind from the cytoplasmic side of the cell membrane (Fig. This contrasts with the case of glibenclamide which has been assumed to act via an intramembrane pathway [38, 39](Fig. The cibenzoline block was enhanced by alkalinization [16].

Although the K channel was first identified in cardiac myocytes [17], its physiological role as a metabo-electrical sensor was first recognized in pancreatic β-cells in terms of insulin secretion. 1 illustrates how β-cells sense extracellular sugar levels and regulate insulin release [18–23].

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