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. 2014 Jun 19;5:95. doi: 10.3389/fendo.2014.00095

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Copyright © 2014 Hiriart, Sanchez-Soto, Diaz-Garcia, Castanares, Avitia, Velasco, Mas-Oliva, Macias-Silva, González-Villalpando, Delgado-Coello, Sosa-Garrocho, Vidaltamayo and Fuentes-Silva.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mechanism of SIR release from hepatocytes. (A) At normal insulin levels, SIR is cleaved from hepatocyte membranes by proteases and passes into the bloodstream, where it retains the ability to bind insulin and also albumin. SIR acts as a physiological carrier for insulin. (B) At hyperinsulinemic conditions, SIR is released and the levels increase in plasma, where it can contribute to insulin resistance by its high affinity binding of the hormone. (C) Proteinase inhibitors, such as alpha2-macroglobulin, modulate SIR release by impeding the cleavage of the insulin receptor within a segment of the beta-domain.