Although hypoglycaemic sulphonylureas have been used to treat non-insulin-dependent diabetes mellitus (NIDDM) for the past forty years, their mechanisms of action at the molecular level have only recently been elucidated. A combination of electrophysiological and molecular biological techniques showed the target of sulphonylureas to be a sulphonylurea receptor (SUR1) and potassium channel (Kir6.2) complex. Together, these two proteins form the ATP-dependent potassium (KATP) channel occurring in insulin- secreting cells. An increase in the blood glucose level triggers a chain of events in insulin-secreting cells and KATP channel closure which is a prerequisite for insulin secretion. In NIDDM, however, an increase in blood glucose fails to close the KATP channel satisfactorily, but this can be remedied by the administration of sulphonylureas.
|Translated title of the contribution||Mechanism of action of oral antidiabetics; Sulphonylureas block ATP-dependent potassium channels|
|Number of pages||5|
|State||Published - Nov 26 1997|
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