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• W1751158548 abstract "Supported in part by NIH grant DK083952. Potential conflict of interest: Nothing to report. Author names in bold designate shared co‐first authorship. Reply: We appreciate Drs. Vinciguerra and Mazzoccoli's comments on our findings about the aryl hydrocarbon receptor/fibroblast growth factor 21 (AHR‐FGF21) endocrine pathway in the dissociation of diet‐induced fatty liver from insulin resistance. We understand that the circadian clock machinery plays an important role in regulating energy balance, and this regulation involves a number of central and peripheral tissues, including the liver. There are a myriad of examples that genetic alterations in clock genes led to metabolic dysfunctions. AHR is a PAS domain transcriptional factor known to play a role in circadian control.1 Indeed, activation of AHR by dioxins has been reported to inhibit clock gene expression and disrupt the circadian clock.1 Therefore, it is possible that the transgenic (TG) activation of AHR in our TG mice could have altered circadian rhythmicity, which might have contributed to the observed metabolic phenotypes. To specifically address the Vinciguerra and Mazzoccoli comments, we measured the hepatic expression of several core clock genes, including Clock, Per1, and Per2, in mice maintained on chow diet or treated with the high‐fat diet (HFD). We found that expression of Clock, Per1, and Per2 was decreased in CA‐AHR TG mice in both the chow‐fed and HFD‐fed conditions (Fig. 1). These results are consistent with the previous reports that TCDD and other xenobiotics could influence circadian gene expression.1 Future studies are necessary to determine whether TG activation of AHR alters the oscillation pattern of clock genes.Figure 1: Activation of AHR suppressed hepatic expression of circadian clock genes. Wild‐type (WT) and CA‐AHR TG mice were fed with chow diet for 14 weeks or HFD for 12 weeks. Shown are the hepatic messenger RNA (mRNA) expressions of Clock, Per1, and Per2 as measured by real‐time polymerase chain reaction.One of our most interesting findings is the establishment of FGF21 as a novel AHR target gene.2 Again, in our animal model, it remains to be determined whether TG activation of AHR alters the circadian rhythmicity and, if so, whether the circadian pattern of FGF21, as an AHR target gene, will be changed. To our knowledge, the circadian regulation of FGF21 and the mechanism of this circadian regulation are not as well established as the fasting‐responsive regulation of FGF21.3 The nocturnal rise of serum FGF21 in humans may be involved in the regulation of glucose homeostasis during the night.4 In principle, the AHR in our TG mice is constitutively activated throughout the day, so it is likely that the sustained increase in circulating FGF21 may have contributed to the metabolic benefits observed in our TG mice. This interpretation is consistent with the reports that chronic administration of recombinant FGF21 protein or TG overexpression of FGF215 was sufficient to confer the metabolic benefits." @default.
• W1751158548 created "2016-06-24" @default.
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• W1751158548 date "2015-08-11" @default.
• W1751158548 modified "2023-09-24" @default.
• W1751158548 title "Reply" @default.
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• W1751158548 doi "https://doi.org/10.1002/hep.27957" @default.
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