1985
DOI: 10.1159/000180105
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Insulin Receptor Regulation in Human Mature Red Cells in vitro

Abstract: We have studied the ability of mature red cells to regulate the number and affinity of their insulin receptors, in vitro. Our data show that mature red cells are not able to change either the number and the affinity of their insulin receptors, after preincubation with high concentrations of insulin alone or insulin and glucose. We conclude that mature red cells possess an insulin receptor system not completely similar to that of major target cells such as hepatocytes and adipocytes, and therefore we suggest so… Show more

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Cited by 3 publications
(2 citation statements)
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“…Indeed, even plasma insulin levels within the normal range were shown to negatively correlate with the hyperemic response of healthy individuals (1). Although impaired vasodilator function of resistance arteries has been reported in some animal models of insulin resistance (14, 15), the effects of hyperinsulinemia on the matching of O 2 supply with the O 2 need in skeletal muscle have not been determined.Since human red blood cells (RBCs) possess insulin receptors (17,18,49), we hypothesized that insulin itself, via the inhibition of ATP release from RBCs, could contribute directly to vascular dysfunction in prediabetes. Insulin, at levels found in humans with prediabetes (38,40,42,44), has been shown to inhibit ATP release from human RBCs in response to an exposure to reduced PO 2 (27).…”
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confidence: 99%
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“…Indeed, even plasma insulin levels within the normal range were shown to negatively correlate with the hyperemic response of healthy individuals (1). Although impaired vasodilator function of resistance arteries has been reported in some animal models of insulin resistance (14, 15), the effects of hyperinsulinemia on the matching of O 2 supply with the O 2 need in skeletal muscle have not been determined.Since human red blood cells (RBCs) possess insulin receptors (17,18,49), we hypothesized that insulin itself, via the inhibition of ATP release from RBCs, could contribute directly to vascular dysfunction in prediabetes. Insulin, at levels found in humans with prediabetes (38,40,42,44), has been shown to inhibit ATP release from human RBCs in response to an exposure to reduced PO 2 (27).…”
mentioning
confidence: 99%
“…Since human red blood cells (RBCs) possess insulin receptors (17,18,49), we hypothesized that insulin itself, via the inhibition of ATP release from RBCs, could contribute directly to vascular dysfunction in prediabetes. Insulin, at levels found in humans with prediabetes (38,40,42,44), has been shown to inhibit ATP release from human RBCs in response to an exposure to reduced PO 2 (27).…”
mentioning
confidence: 99%