The acyl-amino-alkyl benzoic acid residue and the sulfonylurea containing residue of glibenclamide affect different aspects of β-cell function

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Abstract
HB 699 is a non-sulfonylurea acyl-amino bezoic acid derivative, corresponding to a major part of the glibenclamide molecule. Basal insulin release (3 mmol/l glucose) as well as glucose-induced release (10 mmol/l glucose) were stimulated by 25 .mu.mol/l and 200 .mu.mol/l HB 699 in the Ob/ob mouse. HB 699 (200 .mu.mol/l) had no effect on the osmotic swelling induced by hypoosmolarity (180 mosm/l). The glibenclamide-induced insulin release can be resolved in a high-affinity component, which correlates with increased osmotic resistance in the .beta.-cells and a low-affinity component not associated with increased osmotic resistance. The latter component may be due to the part of the glibenclamide molecule that corresponds to HB 699.