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- W1933591708 abstract "Potential conflict of interest: Nothing to report. To the Editor: We read with great interest the article by Lu et al.1 in which the authors demonstrate, using aryl hydrocarbon receptor (AHR, a xenobiotic receptor that senses exogenous toxicants) liver‐specific and inducible transgenic mice fed an obesogenic diet, that activation of the AHR signaling pathway exacerbates hepatic steatosis with a paradoxical protection from obesity and systemic insulin resistance. Moreover, the authors identify fibroblast growth factor 21 (FGF21) as a direct hepatic target of AHR and as the mediator of the systemic metabolic benefits as well as of the hepatic steatosis observed in AHR transgenic mice.1 Although these findings are very impactful, because they establish a new AHR–FGF21 endocrine pathway integrating chemical and nutrient signaling in the liver, there is an important aspect to be stressed. Liver metabolic pathways are driven by circadian biological clocks, and hepatic health is maintained by proper timing of circadian patterns of metabolic gene expression, with the alternation of anabolic processes corresponding to feeding/activity during wake times and catabolic processes characterizing fasting/resting during sleep.2 An intricate relationship has been shown between the clock gene machinery and the AHR signaling pathway.3 The AHR/ARNT protein and the circadian protein BMAL1/ARNTL share structural similarities, and AHR influences the rhythmicity of biological clocks, also through its interaction with BMAL1, the activity of which is altered in AHR knockout mice.4 The AHR has no effects on the biological clock in the absence of exogenous agonist, whereas AHR activation alters circadian rhythmicity and clock gene expression.3 In turn, liver‐produced FGF21 can regulate metabolism and circadian behavior by acting on the nervous system.5 It is plausible that the authors missed interpreting their intriguing mouse phenotype as due to a disruption of the circadian homeostasis as a result of a continuous, time‐disconnected AHR/FGF21 activation. The elegant doxycycline‐inducible transgenic model of Lu et al. would be useful to exploit for time window–restricted experiments of AHR/FGF21 activation. At the patient level, it would be crucial to connect these molecular studies to lifestyle patterns and eventually to chronotherapy based on nontoxic AHR agonists." @default.
- W1933591708 created "2016-06-24" @default.
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- W1933591708 date "2015-08-21" @default.
- W1933591708 modified "2023-09-27" @default.
- W1933591708 title "Aryl hydrocarbon receptor–fibroblast growth factor 21 dissociation of fatty liver from insulin resistance: A timely matter?" @default.
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- W1933591708 doi "https://doi.org/10.1002/hep.27958" @default.
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