Intravenous Glucose Infusion Fails to Alter Monocyte Insulin-Binding Affinity in Normal Subjects

Summary Previous investigations have demonstrated an increase in monocyte insulin receptor affinity two and five hours following oral carbohydrate loading. The present studies were undertaken to see if intravenous (IV) glucose challenge provokes a similar increase in monocyte insulin binding affinit...

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Veröffentlicht in:Hormone and metabolic research 1985-09, Vol.17 (9), p.464-466
Hauptverfasser: Kingston, W. J., Livingston, J. N., Moxley, R. T.
Format: Artikel
Sprache:eng
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Zusammenfassung:Summary Previous investigations have demonstrated an increase in monocyte insulin receptor affinity two and five hours following oral carbohydrate loading. The present studies were undertaken to see if intravenous (IV) glucose challenge provokes a similar increase in monocyte insulin binding affinity. 25 grams of glucose were given to 10 lean normals and monocytes were isolated for 125 I-insulin tracer binding studies (8.4 × 10 -10 M) at 0,1 and 5 hours after glucose loading. The mean data show that monocytes develop a small, statistically insignificant increase in insulin-binding affinity one hour after intravenous glucose (mean ± SEM, 7.28 ± 1.06 ng/ml compared to basal 50% insulin displacement value, B 50 , of 9.25 ± 1.62 ng/ml). B 50 values demonstrated no increase in binding affinity at five hours (10.77 ± 2.22 ng/ml). Prior studies have shown a 50 to 70% decrease in B 50 following oral glucose, indicating a rapid increase in receptor binding affinity after carbohydrate ingestion. In contrast the present studies have shown that after IV glucose six normals had no decrease in B 50 at one or five hours, while the remaining four normals had a 35% decrease at one hour but no decrease at five hours. Intravenous glucose loading, unlike an oral carbohydrate challenge, fails to provoke an acute, consistent increase in monocyte insulin binding affinity at these time points. Elevations in plasma glucose and insulin do not by themselves induce the acute increase in receptor affinity.
ISSN:0018-5043
1439-4286
DOI:10.1055/s-2007-1013577