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Research Article Free access | 10.1172/JCI110817
1Department of Medicine and Research Center, Huddinge Hospital, Karolinska Institute, S-14186 Huddinge, Sweden
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1Department of Medicine and Research Center, Huddinge Hospital, Karolinska Institute, S-14186 Huddinge, Sweden
Find articles by Bolinder, J. in: JCI | PubMed | Google Scholar
1Department of Medicine and Research Center, Huddinge Hospital, Karolinska Institute, S-14186 Huddinge, Sweden
Find articles by Östman, J. in: JCI | PubMed | Google Scholar
Published March 1, 1983 - More info
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.