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. 2022 Nov 22;27:103. doi: 10.1186/s11658-022-00397-7

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© The Author(s) 2022

Open AccessThis 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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Fig. 2 — Pathological role of AhR/CYP1A1 in the pancreas: activation of AhR in the pancreatic islets upon exposure to ligands such as TCDD, leads to induction of CYP1A1, with subsequent generation of ROS and disruption of PKC and mitogen activated protein kinases (MAPK) signaling pathways, resulting in impaired insulin secretion and glucose intolerance within the islet. In addition, AhR–ARNT complexes formed in the pancreas also regulate the expression of specific genes, such as MODY-2 and Akt-2, which are critical to glucose metabolism and hemostasis. Created by bioRender.com