Normal calcium-activated potassium channel in red cells in type 2 diabetes.
The diminished insulin secretion of type 2 diabetes might result from abnormal regulation of the potassium permeability which leads to beta-cell depolarization. The possibility of a generalized defect has been investigated in vitro by the stimulation of 86Rb efflux from red cells of type 2 diabetic patients by calcium ionophore and its inhibition by quinine. Diabetic subjects and control subjects had identical 86Rb efflux stimulated by 0.2-0.6 microM calcium ionophore A23187 and identical inhibition by quinine with mean Ki 6 microM and 4 microM quinine respectively for 0.2 microM ionophore and mean Ki 38 microM and 37 microM quinine respectively for 0.6 microM ionophore.
D000328:Adult; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000502:physiology*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood*; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D008875:Middle Aged; D011188:Potassium / Q000097:blood*; D011803:Quinine / Q000494:pharmacology
D007473:Ion Channels; D000001:Calcimycin; D011803:Quinine; D011188:Potassium; D002118:Calcium