Angiotensin II Inhibits Insulin Binding to Endothelial Cells

BackgroundInsulin-mediated glucose uptake in insulin target tissues is correlated with interstitial insulin concentration, rather than plasma insulin concentration. Therefore, insulin delivery to the interstitium of target tissues is very important, and the endothelium may also play an important rol...

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Main Authors: Su-Jin Oh, Won-Chul Ha, Jee-In Lee, Tae-Seo Sohn, Ji-Hyun Kim, Jung-Min Lee, Sang-Ah Chang, Oak-Kee Hong, Hyun-Shik Son
Format: Article
Language:English
Published: Korean Diabetes Association 2011-06-01
Series:Diabetes & Metabolism Journal
Subjects:
Online Access:http://e-dmj.org/Synapse/Data/PDFData/2004DMJ/dmj-35-243.pdf
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author Su-Jin Oh
Won-Chul Ha
Jee-In Lee
Tae-Seo Sohn
Ji-Hyun Kim
Jung-Min Lee
Sang-Ah Chang
Oak-Kee Hong
Hyun-Shik Son
author_facet Su-Jin Oh
Won-Chul Ha
Jee-In Lee
Tae-Seo Sohn
Ji-Hyun Kim
Jung-Min Lee
Sang-Ah Chang
Oak-Kee Hong
Hyun-Shik Son
author_sort Su-Jin Oh
collection DOAJ
description BackgroundInsulin-mediated glucose uptake in insulin target tissues is correlated with interstitial insulin concentration, rather than plasma insulin concentration. Therefore, insulin delivery to the interstitium of target tissues is very important, and the endothelium may also play an important role in the development of insulin resistance.MethodsAfter treating bovine aortic endothelial cells with angiotensin II (ATII), we observed the changes in insulin binding capacity and the amounts of insulin receptor (IR) on the cell membranes and in the cytosol.ResultsAfter treatment of 10-7M ATII, insulin binding was decreased progressively, up to 60% at 60 minutes (P<0.05). ATII receptor blocker (eprosartan) dose dependently improved the insulin binding capacity which was reduced by ATII (P<0.05). At 200 µM, eprosartan fully restored insulin binding capacity, althogh it resulted in only a 20% to 30% restoration at the therapeutic concentration. ATII did not affect the total amount of IR, but it did reduce the amount of IR on the plasma membrane and increased that in the cytosol.ConclusionATII decreased the insulin binding capacity of the tested cells. ATII did not affect the total amount of IR but did decrease the amount of IR on the plasma membrane. Our data indicate that ATII decreases insulin binding by translocating IR from the plasma membrane to the cytosol. The binding of insulin to IR is important for insulin-induced vasodilation and transendothelial insulin transport. Therefore, ATII may cause insulin resistance through this endothelium-based mechanism.
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spelling doaj.art-112d0c25e91a4a2aa1537ef5c2718d9c2022-12-21T19:20:05ZengKorean Diabetes AssociationDiabetes & Metabolism Journal2233-60792233-60872011-06-0135324324710.4093/dmj.2011.35.3.2432740Angiotensin II Inhibits Insulin Binding to Endothelial CellsSu-Jin OhWon-Chul HaJee-In LeeTae-Seo SohnJi-Hyun KimJung-Min LeeSang-Ah ChangOak-Kee HongHyun-Shik SonBackgroundInsulin-mediated glucose uptake in insulin target tissues is correlated with interstitial insulin concentration, rather than plasma insulin concentration. Therefore, insulin delivery to the interstitium of target tissues is very important, and the endothelium may also play an important role in the development of insulin resistance.MethodsAfter treating bovine aortic endothelial cells with angiotensin II (ATII), we observed the changes in insulin binding capacity and the amounts of insulin receptor (IR) on the cell membranes and in the cytosol.ResultsAfter treatment of 10-7M ATII, insulin binding was decreased progressively, up to 60% at 60 minutes (P<0.05). ATII receptor blocker (eprosartan) dose dependently improved the insulin binding capacity which was reduced by ATII (P<0.05). At 200 µM, eprosartan fully restored insulin binding capacity, althogh it resulted in only a 20% to 30% restoration at the therapeutic concentration. ATII did not affect the total amount of IR, but it did reduce the amount of IR on the plasma membrane and increased that in the cytosol.ConclusionATII decreased the insulin binding capacity of the tested cells. ATII did not affect the total amount of IR but did decrease the amount of IR on the plasma membrane. Our data indicate that ATII decreases insulin binding by translocating IR from the plasma membrane to the cytosol. The binding of insulin to IR is important for insulin-induced vasodilation and transendothelial insulin transport. Therefore, ATII may cause insulin resistance through this endothelium-based mechanism.http://e-dmj.org/Synapse/Data/PDFData/2004DMJ/dmj-35-243.pdfAngiotensin IIAngiotensin II receptor blockerEndotheliumInsulin resistanceTranscapillary insulin transport
spellingShingle Su-Jin Oh
Won-Chul Ha
Jee-In Lee
Tae-Seo Sohn
Ji-Hyun Kim
Jung-Min Lee
Sang-Ah Chang
Oak-Kee Hong
Hyun-Shik Son
Angiotensin II Inhibits Insulin Binding to Endothelial Cells
Diabetes & Metabolism Journal
Angiotensin II
Angiotensin II receptor blocker
Endothelium
Insulin resistance
Transcapillary insulin transport
title Angiotensin II Inhibits Insulin Binding to Endothelial Cells
title_full Angiotensin II Inhibits Insulin Binding to Endothelial Cells
title_fullStr Angiotensin II Inhibits Insulin Binding to Endothelial Cells
title_full_unstemmed Angiotensin II Inhibits Insulin Binding to Endothelial Cells
title_short Angiotensin II Inhibits Insulin Binding to Endothelial Cells
title_sort angiotensin ii inhibits insulin binding to endothelial cells
topic Angiotensin II
Angiotensin II receptor blocker
Endothelium
Insulin resistance
Transcapillary insulin transport
url http://e-dmj.org/Synapse/Data/PDFData/2004DMJ/dmj-35-243.pdf
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AT jihyunkim angiotensiniiinhibitsinsulinbindingtoendothelialcells
AT jungminlee angiotensiniiinhibitsinsulinbindingtoendothelialcells
AT sangahchang angiotensiniiinhibitsinsulinbindingtoendothelialcells
AT oakkeehong angiotensiniiinhibitsinsulinbindingtoendothelialcells
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