[Molecular mechanisms of insulin secretion].

Abstract:

:Insulin secretion from the beta-cells in the islets of Langerhans is mainly regulated by glucose entry via its transporter. The intracellular glucose metabolism induces a rise in ATP/ADP ratio which increases the degree of closure of ATP-sensitive potassium channels (K(ATP) channels), inducing a higher intracellular K+, which, in turn, depolarizes the membrane and opens voltage-sensitive calcium channels. The ensuing Ca2+ entry triggers extrusion of insulin-containing secretory granules and, thus, hormone secretion. The analysis of the structure of the genes encoding K(ATP) channels that are made of four Kir subunits (forming the ionic pore) and four regulatory SUR subunits (that contain the binding site for antidiabetic sulfonylureas) allowed to several subclasses of those ionic channels to be described: Insulin secreting beta cells contain the SUR1/Kir 6.2 complex, while heart and skeletal muscles contain the SUR2A/Kir 6.2 set, vascular smooth muscles (such as those present in coronary arteries) have SUR2B/Kir 6.1 and nonvascular smooth muscle SUR2B/Kir 6.2. The pharmacological specificity of each sulfonylurea depends on the type of SUR protein present in each tissue: most of the second generation sulfonylureas used in diabetic clinics (e.g. glibenclamide, glimepiride) display almost the same affinity for SUR1 SUR2A and SUR2B, leading to possible harmful adverse effects in type 2 diabetic patients with an associated cardiovascular pathology. In contrast, among the second generation sulfonylureas, only gliclazide displays a remarkable specificity towards the beta-cell K(ATP) channels, making this drug particularly safe in all situations, as it does not induce any interference with the cardiovascular system.

journal_name

Diabetes Metab

journal_title

Diabetes & metabolism

authors

Bataille D

subject

Has Abstract

pub_date

2002-12-01 00:00:00

pages

4S7-13

issue

6 Suppl

eissn

1262-3636

issn

1878-1780

pii

MDOI-DM-12-2002-28-SUPPLEMENT-1262-3636-101019-ART

journal_volume

28

pub_type

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