Novel effect of insulin

Insulin-stimulated Na+ transport is mediated by hydrolysis of phosphoinositides

Carlos M Isales, Lawrence J. MacAla, Jose Rodriguez-Commes, Jose Gasalla-Herraiz, John P. Hayslett

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Previous studies showed that insulin stimulation of electrogenic Na+ transport in renal epithelial cells is mediated by a calcium-dependent signal transduction mechanism. The present study was performed to determine whether the insulin-induced increase in intracellular Ca2+ (Ca(i)2+) was mediated by hydrolysis of phosphatidylinositol and release of inositol trisphosphate. Experiments were conducted with cultured A6 cells, derived from Xenopus laevis, grown on permeable supports. Addition of insulin resulted in 2 to 3 fold increases in inositol trisphosphate and a 50% increase in 1,2 diacylglycerol within 10s, which corresponded to the time-course, previously reported, of insulin stimulated increases in Na+ transport and Ca(i)2+. Further studies showed that aldosterone, previously shown to stimulate an increase in 1,4,5-inositol trisphosphate at onset of the rise in Na+ transport, also increased DAG levels during the initial phase of stimulation of Na+ transport. These studies provide the first evidence that a biological response induced by insulin is mediated by hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) which results in two products, inositol trisphosphate which causes the release of Ca2+ from intracellular stores and 1,2 diacylglycerol. In addition this study provides further support for the proposal that a common signal transduction mechanism mediates electrogenic Na+ transport by multiple agonists.

Original languageEnglish (US)
Pages (from-to)156-159
Number of pages4
JournalBiochemical and Biophysical Research Communications
Volume231
Issue number1
DOIs
StatePublished - Feb 3 1997

Fingerprint

Phosphatidylinositols
Hydrolysis
Insulin
Inositol
Signal transduction
Signal Transduction
Inositol 1,4,5-Trisphosphate
Xenopus laevis
Aldosterone
Cultured Cells
Epithelial Cells
Calcium
Kidney
Experiments
1,2-diacylglycerol

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

Novel effect of insulin : Insulin-stimulated Na+ transport is mediated by hydrolysis of phosphoinositides. / Isales, Carlos M; MacAla, Lawrence J.; Rodriguez-Commes, Jose; Gasalla-Herraiz, Jose; Hayslett, John P.

In: Biochemical and Biophysical Research Communications, Vol. 231, No. 1, 03.02.1997, p. 156-159.

Research output: Contribution to journalArticle

Isales, Carlos M ; MacAla, Lawrence J. ; Rodriguez-Commes, Jose ; Gasalla-Herraiz, Jose ; Hayslett, John P. / Novel effect of insulin : Insulin-stimulated Na+ transport is mediated by hydrolysis of phosphoinositides. In: Biochemical and Biophysical Research Communications. 1997 ; Vol. 231, No. 1. pp. 156-159.
@article{b0f5e0edf3314067a19494b1c5a86e7c,
title = "Novel effect of insulin: Insulin-stimulated Na+ transport is mediated by hydrolysis of phosphoinositides",
abstract = "Previous studies showed that insulin stimulation of electrogenic Na+ transport in renal epithelial cells is mediated by a calcium-dependent signal transduction mechanism. The present study was performed to determine whether the insulin-induced increase in intracellular Ca2+ (Ca(i)2+) was mediated by hydrolysis of phosphatidylinositol and release of inositol trisphosphate. Experiments were conducted with cultured A6 cells, derived from Xenopus laevis, grown on permeable supports. Addition of insulin resulted in 2 to 3 fold increases in inositol trisphosphate and a 50{\%} increase in 1,2 diacylglycerol within 10s, which corresponded to the time-course, previously reported, of insulin stimulated increases in Na+ transport and Ca(i)2+. Further studies showed that aldosterone, previously shown to stimulate an increase in 1,4,5-inositol trisphosphate at onset of the rise in Na+ transport, also increased DAG levels during the initial phase of stimulation of Na+ transport. These studies provide the first evidence that a biological response induced by insulin is mediated by hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) which results in two products, inositol trisphosphate which causes the release of Ca2+ from intracellular stores and 1,2 diacylglycerol. In addition this study provides further support for the proposal that a common signal transduction mechanism mediates electrogenic Na+ transport by multiple agonists.",
author = "Isales, {Carlos M} and MacAla, {Lawrence J.} and Jose Rodriguez-Commes and Jose Gasalla-Herraiz and Hayslett, {John P.}",
year = "1997",
month = "2",
day = "3",
doi = "10.1006/bbrc.1997.6063",
language = "English (US)",
volume = "231",
pages = "156--159",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Academic Press Inc.",
number = "1",

}

TY - JOUR

T1 - Novel effect of insulin

T2 - Insulin-stimulated Na+ transport is mediated by hydrolysis of phosphoinositides

AU - Isales, Carlos M

AU - MacAla, Lawrence J.

AU - Rodriguez-Commes, Jose

AU - Gasalla-Herraiz, Jose

AU - Hayslett, John P.

PY - 1997/2/3

Y1 - 1997/2/3

N2 - Previous studies showed that insulin stimulation of electrogenic Na+ transport in renal epithelial cells is mediated by a calcium-dependent signal transduction mechanism. The present study was performed to determine whether the insulin-induced increase in intracellular Ca2+ (Ca(i)2+) was mediated by hydrolysis of phosphatidylinositol and release of inositol trisphosphate. Experiments were conducted with cultured A6 cells, derived from Xenopus laevis, grown on permeable supports. Addition of insulin resulted in 2 to 3 fold increases in inositol trisphosphate and a 50% increase in 1,2 diacylglycerol within 10s, which corresponded to the time-course, previously reported, of insulin stimulated increases in Na+ transport and Ca(i)2+. Further studies showed that aldosterone, previously shown to stimulate an increase in 1,4,5-inositol trisphosphate at onset of the rise in Na+ transport, also increased DAG levels during the initial phase of stimulation of Na+ transport. These studies provide the first evidence that a biological response induced by insulin is mediated by hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) which results in two products, inositol trisphosphate which causes the release of Ca2+ from intracellular stores and 1,2 diacylglycerol. In addition this study provides further support for the proposal that a common signal transduction mechanism mediates electrogenic Na+ transport by multiple agonists.

AB - Previous studies showed that insulin stimulation of electrogenic Na+ transport in renal epithelial cells is mediated by a calcium-dependent signal transduction mechanism. The present study was performed to determine whether the insulin-induced increase in intracellular Ca2+ (Ca(i)2+) was mediated by hydrolysis of phosphatidylinositol and release of inositol trisphosphate. Experiments were conducted with cultured A6 cells, derived from Xenopus laevis, grown on permeable supports. Addition of insulin resulted in 2 to 3 fold increases in inositol trisphosphate and a 50% increase in 1,2 diacylglycerol within 10s, which corresponded to the time-course, previously reported, of insulin stimulated increases in Na+ transport and Ca(i)2+. Further studies showed that aldosterone, previously shown to stimulate an increase in 1,4,5-inositol trisphosphate at onset of the rise in Na+ transport, also increased DAG levels during the initial phase of stimulation of Na+ transport. These studies provide the first evidence that a biological response induced by insulin is mediated by hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) which results in two products, inositol trisphosphate which causes the release of Ca2+ from intracellular stores and 1,2 diacylglycerol. In addition this study provides further support for the proposal that a common signal transduction mechanism mediates electrogenic Na+ transport by multiple agonists.

UR - http://www.scopus.com/inward/record.url?scp=0031550558&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031550558&partnerID=8YFLogxK

U2 - 10.1006/bbrc.1997.6063

DO - 10.1006/bbrc.1997.6063

M3 - Article

VL - 231

SP - 156

EP - 159

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 1

ER -