Glatt M, Schatz H
Diabete Metab. 1981 Jun;7(2):105-8.
HB 699 belongs to a new class of hypoglycaemic agents, the acyl-amino-alcyl-benzoic acids. Its influence on bion-synthesis and secretion of insulin was studied in collagenase-isolated rat islets. During incubations for 3 hours together with 3H-leucine at 1 and 2 mg/ml glucose, HB 699 (10 micrograms/ml) reduced biosynthesis of proinsulin and insulin (3H-leucine incorporation), whereas insulin release was stimulated. During an incubation period of 2 hours in the absence of glucose, insulin release was enhanced both by HB 699 (50 micrograms/ml) and glibenclamide (10 micrograms/ml). At 1 mg/ml glucose, no additive or potentiating effect of HB 699 to that of glibenclamide was found regarding insulin release. When calcium ions were omitted insulin output in the presence of HB 699 and glucose was reduced. In conclusion, HB 699, although not belonging to the class of sulfonylureas, behaves very similar to these drugs concerning its influence on insulin biosynthesis and secretion in vitro. It acts as an initiator of insulin release, involving probably similar mechanisms as sulfonylureas do.
HB 699属于一类新型的降血糖药物,即酰基氨基烷基苯甲酸类。在胶原酶分离的大鼠胰岛中研究了其对胰岛素生物合成和分泌的影响。在1和2mg/ml葡萄糖浓度下与3H-亮氨酸一起孵育3小时期间,HB 699(10微克/毫升)降低了胰岛素原和胰岛素的生物合成(3H-亮氨酸掺入),而胰岛素释放受到刺激。在无葡萄糖的孵育期2小时内,HB 699(50微克/毫升)和格列本脲(10微克/毫升)均增强了胰岛素释放。在1mg/ml葡萄糖浓度下,未发现HB 699对格列本脲的胰岛素释放有相加或增强作用。当省略钙离子时,在有HB 699和葡萄糖存在的情况下胰岛素分泌减少。总之,HB 699虽然不属于磺脲类药物,但其在体外对胰岛素生物合成和分泌的影响与这些药物非常相似。它作为胰岛素释放的启动剂,可能涉及与磺脲类药物类似的机制。