Abstract
Exposure of microdissected pancreatic islets from obese-hyperglycemic mice to albumin resulted in a depression of both the islet uptake and insulin-releasing action of glibenclamide. The uptake was proportionately more reduced at lower medium concentrations of glibenclamide, reflecting different kinetics for its binding to islets and serum albumin. Whereas phenyl-butazone, sulfonamides, and other sulfonylureas had no influence on the islet uptake of glibenclamide in the absence of albumin, these compounds increased the amounts of glibenclamide bound to islets incubated in albumin-containing medium. When combined with phenylbutazone, glibenclamide stimulated insulin release even at a high albumin concentration. The results are compatible with the idea that drug potentiation of the hypoglycemic action of glibenclamide involves translocation of this insulin secretagogje from serum albumin to the pancreatic β cells.
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