HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Delva, P Articles by Lechi, A Search for Related Content PubMed PubMed Citation Articles by Delva, P Articles by Lechi, A

Department of Biomedical and Surgical Sciences, Section of Medicina Interna C, University of Verona, Policlinico GB Rossi, Piazzale LA Scuro, 37134 Verona, Italy

(Requests for offprints should be addressed to P Delva; Email: pietro.delva{at}univr.it)

Insulin is capable of increasing intracellular magnesium, although very little is known about the effect of insulin on the biologically active fraction of magnesium, i.e. the ionized quota (Mg_i²⁺), its interactions with glucose, and the cellular mechanisms involved in these processes. We studied the interactions of the effects of insulin and glucose on intracellular ionized magnesium in human lymphocytes. Mg_i²⁺ was measured using a fluorimetric method and the Mg²⁺-sensitive dye, furaptra. We found that insulin significantly increases the Mg_i²⁺(without insulin 227 ± 14 µM, with 10 µU/ml, insulin 301 ± 30 µM, P<0.0001, n = 12) in a dose-dependent manner in all three glucose concentrations tested (5, 7 and 15 mmol/l). The half-maximal effect of insulin was approximately 0.8 µU/ml. Glucose and insulin showed opposite effects in their ability to modify Mg_i²⁺ in lymphocytes. Inhibitors of the membrane Na⁺- Mg²⁺ transport system and of phosphatidylinositol (PI) 3-kinase abolish the insulin-mediated increase of Mg_i²⁺, thus suggesting that insulin is capable of increasing Mg_i²⁺ by modulating the activity of this transport system, possibly through the mediation of PI 3-kinase activation. Taking into account the relationship between insulin and glucose plasma levels and their opposing effects on Mg_i²⁺, this mechanism may represent the two limbs of a biphasic regulatory system of Mg_i²⁺ in both physiological and pathological conditions.