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Research Article Free access | 10.1172/JCI110817

Marked Increase in Insulin Sensitivity of Human Fat Cells 1 Hour after Glucose Ingestion

Peter Arner, Jan Bolinder, and Jan Östman

1Department of Medicine and Research Center, Huddinge Hospital, Karolinska Institute, S-14186 Huddinge, Sweden

Find articles by Arner, P. in: PubMed | Google Scholar

1Department of Medicine and Research Center, Huddinge Hospital, Karolinska Institute, S-14186 Huddinge, Sweden

Find articles by Bolinder, J. in: PubMed | Google Scholar

1Department of Medicine and Research Center, Huddinge Hospital, Karolinska Institute, S-14186 Huddinge, Sweden

Find articles by Östman, J. in: PubMed | Google Scholar

Published March 1, 1983 - More info

Published in Volume 71, Issue 3 on March 1, 1983
J Clin Invest. 1983;71(3):709–714. https://doi.org/10.1172/JCI110817.
© 1983 The American Society for Clinical Investigation
Published March 1, 1983 - Version history
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Abstract

The effect of glucose ingestion on insulin action was investigated in isolated human fat cells. Subcutaneous adipose tissue was obtained from eight normal adult volunteers before and 1 h after oral intake of 100 g of glucose. Lipolysis (glycerol release) and specific insulin receptor binding were determined. Insulin binding increased significantly by 20-30% after glucose ingestion. This was due to an increase in insulin binding affinity, without any change in the receptor number. The concentration of insulin producing half-maximum inhibition (ED50) of basal lipolysis was 50 μU/ml before and 0.25 μU/ml after glucose ingestion (P < 0.01), which represented a 200-fold difference. As regards isoprenaline-induced lipolysis, the ED50 for insulin inhibition was 30 μU/ml before and 2.5 μU/ml after oral glucose (P < 0.01), which was a 12-fold difference. The maximum insulin-induced inhibition of basal and isoprenaline-induced lipolysis were not altered after oral glucose. It is concluded that glucose ingestion is accompanied by a marked increase in insulin sensitivity of human fat cells and this may be an important modulating factor in the overall scheme of insulin action.

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