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Effect of PGE2 on sulfonylurea induced insulin release.

A. Villar, Ivorra, Elsa Anselmi

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Abstract

1. Previous studies have demonstrated that the administration of prostaglandins (PGs) inhibits insulin secretion in vivo and have suggested that these compounds may be involved in the pathogenesis of diabetes mellitus. The present study was carried out in order to explore the effect of PGE2 on sulfonylurea-induced insulin release. 2. We determined glycemia and insulinemia in rat blood samples, at different times before and after the intraarterial administration of: (a) glibenclamide, (b) tolbutamide, (c) PGE2, (d) glibenclamide and PGE2, (e) tolbutamide and PGE2; in all cases with and without a glucose pulse. (Glibenclamide 0.5 mg/kg, tolbutamide 50 mg/kg, PGE2 100 micrograms/kg and glucose 500 mg/kg). 3. The results of these experiments demonstrate that PGE2 partially inhibits sulfonylurea-induced insulin release. The plasma insulin and glucose levels remain within the range of intermediate values as compared to the control groups (sulfonylurea or PGE2-treated rats) both in presence and absence of glucose.

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1. Previous studies have demonstrated that the administration of prostaglandins (PGs) inhibits insulin secretion in vivo and have suggested that these compounds may be involved in the pathogenesis of diabetes mellitus. The present study was carried out in order to explore the effect of PGE2 on sulfonylurea-induced insulin release. 2. We determined glycemia and insulinemia in rat blood samples, at different times before and after the intraarterial administration of: (a) glibenclamide, (b) tolbutamide, (c) PGE2, (d) glibenclamide and PGE2, (e) tolbutamide and PGE2; in all cases with and without a glucose pulse. (Glibenclamide 0.5 mg/kg, tolbutamide 50 mg/kg, PGE2 100 micrograms/kg and glucose 500 mg/kg). 3. The results of these experiments demonstrate that PGE2 partially inhibits sulfonylurea-induced insulin release. The plasma insulin and glucose levels remain within the range of intermediate values as compared to the control groups (sulfonylurea or PGE2-treated rats) both in presence and absence of glucose.

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Available abstract

1. Previous studies have demonstrated that the administration of prostaglandins (PGs) inhibits insulin secretion in vivo and have suggested that these compounds may be involved in the pathogenesis of diabetes mellitus. The present study was carried out in order to explore the effect of PGE2 on sulfonylurea-induced insulin release. 2. We determined glycemia and insulinemia in rat blood samples, at different times before and after the intraarterial administration of: (a) glibenclamide, (b) tolbutamide, (c) PGE2, (d) glibenclamide and PGE2, (e) tolbutamide and PGE2; in all cases with and without a glucose pulse. (Glibenclamide 0.5 mg/kg, tolbutamide 50 mg/kg, PGE2 100 micrograms/kg and glucose 500 mg/kg). 3. The results of these experiments demonstrate that PGE2 partially inhibits sulfonylurea-induced insulin release. The plasma insulin and glucose levels remain within the range of intermediate values as compared to the control groups (sulfonylurea or PGE2-treated rats) both in presence and absence of glucose.

Key concepts: Glibenclamide, Tolbutamide, Sulfonylurea, Insulin, Internal medicine, Endocrinology, Diabetes mellitus, In vivo

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