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. 2016 May 5;11(5):e0154415. doi: 10.1371/journal.pone.0154415

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© 2016 Bertuzzi et al

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Fig 6 — (A- C) Model predictions of $A k t_{n}^{T}, A k t_{n}^{S}$ , and $A k t_{n}^{T, S}$ at 1 and 100 nM insulin in control (white boxes) and in cells exposed to UCN-01 (black boxes), obtained by a tenfold decrease of the PDK1 parameter a₉. The plots show the marked decrease of $A k t_{n}^{T}$ and $A k t_{n}^{T, S}$ , with the resulting increase in $A k t_{n}^{S}$ in treated cells compared to control. (D) The model prediction of GLUT4 concentration at plasma membrane highlights the insulin resistance elicited by the drug. (E) S6K1_n reduction due to drug action on PDK1. (F) $I R S 1_{n}^{Y}$ enhancement caused by the weakening of negative feedback.