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. 2020 Dec 10;10:21628. doi: 10.1038/s41598-020-78376-1

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© The Author(s) 2020

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Activation of IκBα and mTORC1 caused by palmitate in podocytes and diabetic glomeruli. Expression of phospho-NF-κB, NF-κB, phospho-IκBα (ser32/36), IκBα, phospho-mTOR (ser2448), mTOR, phospho-S6 (ser240/244), S6, phospho-JNK, JNK, PKCα, PKCβ, PKCδ, PKCε, PKCζ, cadherin and actin were detected by immunoblot and densitometry quantitation was measured from (a, b, c, d) mouse podocytes exposed to palmitate for 24 h as well as from (e, f) isolated glomeruli at 25 weeks of age of nondiabetic db/dm and diabetic db/db mice. Results are shown as mean ± SD of 4 (a, b, c, d) independent experience and 6 (e, f) mice per group.