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
Hauptverfasser: McElduff, A., Chipps, D. R., Eastman, C. J.
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container_title Hormone and metabolic research
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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.
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Initial insulin receptor binding correlated strongly with the subsequent decline in plasma glucose concentration (r = 0.9527; P &lt; 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. 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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 &lt; 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 &lt; 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. 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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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