The Erythrocyte Insulin Receptor Response to Insulin Induced Hypoglycaemia
Summary The response of the erythrocyte insulin receptor to a prolonged intravenous infusion of insulin has been measured in normal individuals during hypoglycaemia and when hypoglycaemia was prevented by the concurrent infusion of glucose. When euglycaemia was maintained, mean (± S.D.) specific ins...
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Veröffentlicht in: | Hormone and metabolic research 1986-07, Vol.18 (7), p.462-465 |
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creator | McElduff, A. Chipps, D. R. Eastman, C. J. |
description | Summary
The response of the erythrocyte insulin receptor to a prolonged intravenous infusion of insulin has been measured in normal individuals during hypoglycaemia and when hypoglycaemia was prevented by the concurrent infusion of glucose. When euglycaemia was maintained, mean (± S.D.) specific insulin binding following the 5 hour insulin infusion was unchanged (6.9±2.1 to 6.65±2.2% bound per 2.25 × 10
9
erythrocytes). In the presence of mild hypoglycaemia, mean (±SD) specific insulin binding rose from 6.6±2.3 to 7.6±2.5% bound per 2.25 × 10
9
erythrocytes (P < 0.01), after 5 hours. This increase was due to increased receptor affinity. It was not correlated with the increase in the concentration of any individual counter-regulatory hormone. Initial insulin receptor binding correlated strongly with the subsequent decline in plasma glucose concentration (r = 0.9527; P < 0.01). Thus, acute hyperinsulinaemia, when associated with hypoglycaemia, does not result in downregulation of insulin receptors on erythrocytes but rather results in increased receptor binding. Consequently, the insulin receptor may not play an active role in protecting the individual against acute hypoglycaemia. |
doi_str_mv | 10.1055/s-2007-1012346 |
format | Article |
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The response of the erythrocyte insulin receptor to a prolonged intravenous infusion of insulin has been measured in normal individuals during hypoglycaemia and when hypoglycaemia was prevented by the concurrent infusion of glucose. When euglycaemia was maintained, mean (± S.D.) specific insulin binding following the 5 hour insulin infusion was unchanged (6.9±2.1 to 6.65±2.2% bound per 2.25 × 10
9
erythrocytes). In the presence of mild hypoglycaemia, mean (±SD) specific insulin binding rose from 6.6±2.3 to 7.6±2.5% bound per 2.25 × 10
9
erythrocytes (P < 0.01), after 5 hours. This increase was due to increased receptor affinity. It was not correlated with the increase in the concentration of any individual counter-regulatory hormone. Initial insulin receptor binding correlated strongly with the subsequent decline in plasma glucose concentration (r = 0.9527; P < 0.01). Thus, acute hyperinsulinaemia, when associated with hypoglycaemia, does not result in downregulation of insulin receptors on erythrocytes but rather results in increased receptor binding. Consequently, the insulin receptor may not play an active role in protecting the individual against acute hypoglycaemia.</description><identifier>ISSN: 0018-5043</identifier><identifier>EISSN: 1439-4286</identifier><identifier>DOI: 10.1055/s-2007-1012346</identifier><identifier>PMID: 3527927</identifier><identifier>CODEN: HMMRA2</identifier><language>eng</language><publisher>Stuttgart: Thieme</publisher><subject>Adult ; Biological and medical sciences ; Blood Glucose - analysis ; Clinical ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Erythrocytes - metabolism ; Female ; Humans ; Hypoglycemia - blood ; Infusions, Parenteral ; Insulin - blood ; Insulin - metabolism ; Insulin - pharmacology ; Male ; Medical sciences ; Receptor, Insulin - metabolism ; Tumors. Hypoglycemia</subject><ispartof>Hormone and metabolic research, 1986-07, Vol.18 (7), p.462-465</ispartof><rights>Georg Thieme Verlag, Stuttgart · New York</rights><rights>1987 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2726-b74c14b0e3af84f201236d572f87c1cdf325be4836a9add21e57ca8166623b923</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.thieme-connect.de/products/ejournals/pdf/10.1055/s-2007-1012346.pdf$$EPDF$$P50$$Gthieme$$H</linktopdf><link.rule.ids>314,776,780,3004,3005,27901,27902,54534</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8023256$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3527927$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McElduff, A.</creatorcontrib><creatorcontrib>Chipps, D. R.</creatorcontrib><creatorcontrib>Eastman, C. J.</creatorcontrib><title>The Erythrocyte Insulin Receptor Response to Insulin Induced Hypoglycaemia</title><title>Hormone and metabolic research</title><addtitle>Horm Metab Res</addtitle><description>Summary
The response of the erythrocyte insulin receptor to a prolonged intravenous infusion of insulin has been measured in normal individuals during hypoglycaemia and when hypoglycaemia was prevented by the concurrent infusion of glucose. When euglycaemia was maintained, mean (± S.D.) specific insulin binding following the 5 hour insulin infusion was unchanged (6.9±2.1 to 6.65±2.2% bound per 2.25 × 10
9
erythrocytes). In the presence of mild hypoglycaemia, mean (±SD) specific insulin binding rose from 6.6±2.3 to 7.6±2.5% bound per 2.25 × 10
9
erythrocytes (P < 0.01), after 5 hours. This increase was due to increased receptor affinity. It was not correlated with the increase in the concentration of any individual counter-regulatory hormone. Initial insulin receptor binding correlated strongly with the subsequent decline in plasma glucose concentration (r = 0.9527; P < 0.01). Thus, acute hyperinsulinaemia, when associated with hypoglycaemia, does not result in downregulation of insulin receptors on erythrocytes but rather results in increased receptor binding. Consequently, the insulin receptor may not play an active role in protecting the individual against acute hypoglycaemia.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - analysis</subject><subject>Clinical</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Erythrocytes - metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>Hypoglycemia - blood</subject><subject>Infusions, Parenteral</subject><subject>Insulin - blood</subject><subject>Insulin - metabolism</subject><subject>Insulin - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Receptor, Insulin - metabolism</subject><subject>Tumors. Hypoglycemia</subject><issn>0018-5043</issn><issn>1439-4286</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1986</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kM9LwzAYhoMoc06v3oQexFtmfjVpjyLTTQaCzHNI06-uo21q0h7639uxspunJLxP3u_jQeiekiUlcfwcMCNEYUoo40JeoDkVPMWCJfISzQmhCY6J4NfoJoTD-BQpFTM04zFTKVNz9LHbQ7TyQ7f3zg4dRJsm9FXZRF9goe2cHy-hdU2AqHPncNPkvYU8Wg-t-6kGa6AuzS26KkwV4G46F-j7bbV7XePt5_vm9WWLLVNM4kwJS0VGgJsiEQU7Li7zWLEiUZbavOAszkAkXJrU5DmjECtrEiqlZDxLGV-gp1Nv691vD6HTdRksVJVpwPVBK5mmCWF0BJcn0HoXgodCt76sjR80JfooTwd9lKcneeOHh6m5z2rIz_hka8wfp9wEa6rCm8aW4YyNQ8fdjzX4hHX7EmrQB9f7ZjTy39g_CYmD9g</recordid><startdate>198607</startdate><enddate>198607</enddate><creator>McElduff, A.</creator><creator>Chipps, D. R.</creator><creator>Eastman, C. J.</creator><general>Thieme</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>198607</creationdate><title>The Erythrocyte Insulin Receptor Response to Insulin Induced Hypoglycaemia</title><author>McElduff, A. ; Chipps, D. R. ; Eastman, C. J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2726-b74c14b0e3af84f201236d572f87c1cdf325be4836a9add21e57ca8166623b923</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1986</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - analysis</topic><topic>Clinical</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Erythrocytes - metabolism</topic><topic>Female</topic><topic>Humans</topic><topic>Hypoglycemia - blood</topic><topic>Infusions, Parenteral</topic><topic>Insulin - blood</topic><topic>Insulin - metabolism</topic><topic>Insulin - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Receptor, Insulin - metabolism</topic><topic>Tumors. Hypoglycemia</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McElduff, A.</creatorcontrib><creatorcontrib>Chipps, D. R.</creatorcontrib><creatorcontrib>Eastman, C. J.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Hormone and metabolic research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McElduff, A.</au><au>Chipps, D. R.</au><au>Eastman, C. J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Erythrocyte Insulin Receptor Response to Insulin Induced Hypoglycaemia</atitle><jtitle>Hormone and metabolic research</jtitle><addtitle>Horm Metab Res</addtitle><date>1986-07</date><risdate>1986</risdate><volume>18</volume><issue>7</issue><spage>462</spage><epage>465</epage><pages>462-465</pages><issn>0018-5043</issn><eissn>1439-4286</eissn><coden>HMMRA2</coden><abstract>Summary
The response of the erythrocyte insulin receptor to a prolonged intravenous infusion of insulin has been measured in normal individuals during hypoglycaemia and when hypoglycaemia was prevented by the concurrent infusion of glucose. When euglycaemia was maintained, mean (± S.D.) specific insulin binding following the 5 hour insulin infusion was unchanged (6.9±2.1 to 6.65±2.2% bound per 2.25 × 10
9
erythrocytes). In the presence of mild hypoglycaemia, mean (±SD) specific insulin binding rose from 6.6±2.3 to 7.6±2.5% bound per 2.25 × 10
9
erythrocytes (P < 0.01), after 5 hours. This increase was due to increased receptor affinity. It was not correlated with the increase in the concentration of any individual counter-regulatory hormone. Initial insulin receptor binding correlated strongly with the subsequent decline in plasma glucose concentration (r = 0.9527; P < 0.01). Thus, acute hyperinsulinaemia, when associated with hypoglycaemia, does not result in downregulation of insulin receptors on erythrocytes but rather results in increased receptor binding. Consequently, the insulin receptor may not play an active role in protecting the individual against acute hypoglycaemia.</abstract><cop>Stuttgart</cop><cop>New York, NY</cop><pub>Thieme</pub><pmid>3527927</pmid><doi>10.1055/s-2007-1012346</doi><tpages>4</tpages></addata></record> |
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subjects | Adult Biological and medical sciences Blood Glucose - analysis Clinical Endocrine pancreas. Apud cells (diseases) Endocrinopathies Erythrocytes - metabolism Female Humans Hypoglycemia - blood Infusions, Parenteral Insulin - blood Insulin - metabolism Insulin - pharmacology Male Medical sciences Receptor, Insulin - metabolism Tumors. Hypoglycemia |
title | The Erythrocyte Insulin Receptor Response to Insulin Induced Hypoglycaemia |
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