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. 2018 Feb 13;8:2952. doi: 10.1038/s41598-018-21087-5

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fasudil improved vascular insulin signaling in db/db versus db/+ mice, and this is MR-independent pathway. Fasudil treatment prevents increased Ser-307-phosphorylation of Irs1 (A) and decreased Ser-473 phosphorylation of Akt (B) in mesenteric arteries from db/db vs db/+ mice. However, canrenoate treatment has no effect on the increase in Irs1 phosphorylation (C) neither on the decrease in Akt phosphorylation (D) in db/db mice. Data are presented as mean ± SEM; n = 6 to 8 mice/group. *p < 0.05, **p < 0.01 db/db vs db/+. Irs1: Insulin receptor substrate 1; MRA: MR antagonist canrenoate. Vehicle: saline NaCl 0.9%. Results are expressed mean ± SEM, n = 6–8 mice per group, *p < 0.05, **p < 0.01 db/db vs db/+, ^†p < 0.05, ^††p < 0.01 vehicle vs +fasudil. Irs1: insulin receptor substrate 1; Vehicle: saline NaCl 0.9%.