Key result
Defective regulation of ATP-regulated K+ channels may underlie non-insulin-dependent diabetes mellitus, as these channels control insulin secretion and are blocked by sulfonylureas.
Key points are not available for this paper at this time.
Design
Review
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for KATP defects in diabetes; prospective validation required before any practice change.
Glucose-stimulated insulin secretion from pancreatic Beta-cells is dependent on closure of ATP-regulated K+ channels. These channels are selectively blocked by hypoglycaemic sulfonylureas, compounds used in treatment of non-insulin-dependent diabetes mellitus (NIDDM). This suggests that NIDDM may result from defective K+-channel regulation.
No takes yet. Share an insight, caveat, or question.
Rorsman et al. (1990) studied this question. Defective regulation of ATP-regulated K+ channels may underlie non-insulin-dependent diabetes mellitus, as these channels control insulin secretion and are blocked by sulfonylureas.
Synapse has enriched 10 related papers. Consider them for comparative context: