Enhancement of Insulin Release and Islet Cell Calcium Content by an Acyl-Amino-Alcyl Benzoic Acid Derivative, HB 699

R. Puech; M. Manteghetti; G. Ribes; C. B. Wollheim; M. M. Loubatières-Mariani

doi:10.1055/s-2007-1013432

Hormone and Metabolic Research, Table of Contents

Horm Metab Res 1985; 17(1): 1-4
DOI: 10.1055/s-2007-1013432

ORIGINALS

Basic
© Georg Thieme Verlag, Stuttgart · New York

Enhancement of Insulin Release and Islet Cell Calcium Content by an Acyl-Amino-Alcyl Benzoic Acid Derivative, HB 699

R. Puech¹ , M. Manteghetti¹ , G. Ribes¹ , C. B. Wollheim² , M. M. Loubatières-Mariani¹

¹Laboratoire de Pharmacologie et de Pharmacodynamie, Equipe de Recherche Associée au CNRS no 786, Institut de Biologie, Faculté de Médecine, Montpellier, France
²Institut de Biochimie Clinique, University of Geneva, Geneva, Switzerland

Abstract

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Summary

HB 699, a hypoglycaemic agent which lacks the structural requirements regarded as essential for the insulin releasing action of the sulfonamide group, was studied in isolated rat islets and compared with tolbutamide. In the presence of 8.3 mM glucose for long exposure (24 h) both substances induced an increase of insulin release without altering the islet insulin content. After preloading of the islets to isotopic equilibrium with ⁴⁵Ca⁺⁺ (24 h), HB 699 and tolbutamide induced a significant increase in total exchangeable calcium content parallelled by an increase in insulin release. Both effects could be suppressed by verapamil, a blocker of voltage-sensitive Ca⁺⁺ channels. These results indicate that HB 699, like tolbutamide, stimulates insulin release by increasing Ca⁺⁺ uptake by the B cells.

Key-Words:

Insulin Secretion - Islet Insulin Content - Pancreatic Islets - Islet Calcium Content - HB 699

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