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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. 1 — The proposed pathway for AhR-mediated glucose hemostasis and DM by environmental pollutants. AhR is expressed in various tissues, including the pancreas, liver, and adipose tissues, making it a crucial receptor in many physiological and pathological processes involved in insulin secretion and glucose metabolism. Mechanistically, upon binding of TCDD to AhR, the activated receptor translocates to the nucleus after dissociation from its inhibitory protein HSP90 and XAP2. The activated receptor interacts with type 2 basic helix–loop–helix/PER-ARNT-SIM (bHLH-PAS) protein, AhR nuclear translocator (ARNT). The resulting complex selectively binds to a specific sequence on CYP1A1 DNA. known as the xenobiotic responsive element (XRE), leading to transcriptional induction of specific genes involved in xenobiotic metabolism, such as CYP1A1 and CYP1B1. Induction of AhR downstream targets CYP1A1 and CYP1B1 directly or indirectly induce impaired glucose hemostasis and insulin secretion. Created by bioRender.com