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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Korean Diabetes Association
2011-06-01
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Series: | Diabetes & Metabolism Journal |
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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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id | doaj.art-112d0c25e91a4a2aa1537ef5c2718d9c |
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issn | 2233-6079 2233-6087 |
language | English |
last_indexed | 2024-12-21T01:42:58Z |
publishDate | 2011-06-01 |
publisher | Korean Diabetes Association |
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series | Diabetes & Metabolism Journal |
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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