Cytochrome P450 1B1: An unexpected modulator of liver fatty acid homeostasis

Larsen, Michele Campaigne; Bushkofsky, Justin R; Gorman, Tyler; Adhami, Vaqar M.; Mukhtar, Hasan; Wang, Haihui; Reeder, Scott B.; Jefcoate, Colin R.

doi:10.1016/j.abb.2015.02.010

Cited by 46 publications

(88 citation statements)

References 96 publications

(133 reference statements)

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“…We operationally define DIO as an increase in body weight (BW) and adiposity in mice on the HFD relative to equivalent mice on the LFD [29, 30]. GVAD-HFD decreased DIO and liver weight (Figure 2C, D, and F).…”

Section: Resultsmentioning

confidence: 99%

“…Selections of previously reported liver gene responses to the BD-HFD compared to an approximately isocaloric low fat diet (LFD) were used in comparative analyses [29, 30]. …”

Section: Methodsmentioning

confidence: 99%

“…DIO is recognized by increased weight gain and adipose deposition with the HFD relative to the LFD [29, 30]. The DIO changes in males only appear at maturity (approximately diet week 5), at the same time that the GVAD protocol starts to decrease serum retinol.…”

Section: Introductionmentioning

confidence: 99%

“…Mice in which Cyp1b1 is deleted exhibit suppressed DIO [29, 30]. We have identified genes that responded to Cyp1b1 deletion and the difference in diet, HFD versus LFD [30], including gene clusters that did not respond to Cyp1b1 deletion and also those that responded to the diet difference to the same extent in wild type and Cyp1b1-/- mice, which we refer to as HF genes.…”

Section: Introductionmentioning

confidence: 99%

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Diet-dependent retinoid effects on liver gene expression include stellate and inflammation markers and parallel effects of the nuclear repressor Shp

Maguire

Bushkofsky

Larsen

et al. 2017

The Journal of Nutritional Biochemistry

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For mice, a maternal vitamin A (VA) deficient diet initiated from mid-gestation (GVAD) produces serum retinol deficiency in mature offspring. We hypothesize that the effects of GVAD arise from pre-weaning developmental changes. We compare the effect of this GVAD protocol in combination with a post-weaning high fat diet (HFD) or high carbohydrate diet (LF12). Each is compared to an equivalent VA sufficient combination. GVAD extensively decreased serum retinol and liver retinol, retinyl esters, and retinoid homeostasis genes (Lrat, Cyp26b1, and Cyp26a1). These suppressions were each more effective with LF12 than with HFD. Post-weaning initiation of VA deficiency with LF12 depleted liver retinoids, but serum retinol was unaffected. Liver retinoid depletion, therefore, precedes serum attenuation. Maternal LF12 decreased the obesity response to the HFD, which was further decreased by GVAD. LF12 fed to the mother and offspring extensively stimulated genes marking stellate activation (Col1a1, Timp2, and Cyp1b1) and novel inflammation markers (Ly6d, Trem2, Nupr1). The GVAD with LF12 diet combination suppressed these responses. GVAD in combination with the HFD increased these same clusters. A further set of expression differences on the HFD when compared to a high carbohydrate diet were prevented when GVAD was combined with HFD. Most of these GVAD gene changes match published effects from deletion of Nr0b2/Shp, a retinoid-responsive, nuclear co-repressor that modulates metabolic homeostasis. The stellate and inflammatory increases seen with the high carbohydrate, LF12 diet may represent postprandial responses. They depend on retinol and Shp, but the regulation reverses with a HFD.

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Section: Resultsmentioning

confidence: 99%

“…Selections of previously reported liver gene responses to the BD-HFD compared to an approximately isocaloric low fat diet (LFD) were used in comparative analyses [29, 30]. …”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Diet-dependent retinoid effects on liver gene expression include stellate and inflammation markers and parallel effects of the nuclear repressor Shp

Maguire

Bushkofsky

Larsen

et al. 2017

The Journal of Nutritional Biochemistry

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“…Recently microarray data from the livers of the CYP1B1 KO mice that are resistant to diet-induced obesity indicated that CYP1B1 deletion substantially alters the expression of genes associated with fatty acid homeostasis [33]. Several studies have examined the relationship between individual CYP1B1 polymorphisms and cancer risk [14,15,[34][35][36][37].…”

Section: Discussionmentioning

confidence: 99%

Cytochrome P450 Cyp1b1*2 Gene and Its Association With T2d in Tabuk Population, Northwestern Region of Saudi Arabia

Elfaki

Almutairi

Mir

et al. 2018

Asian J Pharm Clin Res

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Objective: Cytochrome P450 1B1 (CYP1B1) is involved in the activation of procarcinogens and steroid metabolism. Genetic variants of CYP1B1 are associated with altered catalytic activity and disease phenotypes. The purpose of this study was to investigate the role of CYP1B1 (rs1056827) polymorphism in inducing T2D. Methods:This cross-sectional study enrolled 113 subjects of T2D and 120 controls. DNA was isolated from blood. Genotyping of the rs1056827 was done by allele-specific polymerase chain reaction. The frequency of alleles and genotype distribution was compared in T2D cases and healthy controls. Statistical analysis was performed with SPSS, Chi-square, and Fisher exact test. Hardy-Weinberg equilibrium was tested by a χ 2 test. The associations between rs1056827 variant genotypes and T2D were estimated by computing the odds ratios and their 95% confidence intervals (CI) from univariate and multivariate logistic regression analysis.Results: A significant association of rs1056827 was found between T2D cases and controls (p<0.0001). When GG genotype was compared with GT genotype a significant association was found with odd ration ( Conclusion:This result suggests a significant association between rs1056827G>T polymorphism and T2D. This finding is limited due to the smaller sample size and can be validated by large sample size studies.

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A rapid method of preparing complex organohalogen extracts from avian eggs: Applications to in vitro toxicogenomics screening

Crump

Williams

Chiu

et al. 2019

Enviro Toxic and Chemistry

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Double‐crested cormorants are piscivorous birds that breed in variably contaminated colonies across the Laurentian Great Lakes of North America. Collection and preparation of environmentally relevant extracts from eggs that contain variable concentrations of organohalogen contaminants represents a minimally invasive approach to characterize potential effects of exposure using in vitro bioassays. In the present study, a rapid, efficient lipid freeze‐filtration extraction method was used to prepare extracts from double‐crested cormorant eggs collected from 5 breeding colonies that had variable organohalogen contaminant burdens. Extracts, solubilized in dimethyl sulfoxide, were administered to chicken embryonic hepatocytes (CEHs) to determine effects on cell viability, 7‐ethoxyresorufin‐O‐deethylase (EROD) activity, and messenger RNA expression using a chicken ToxChip polymerase chain reaction (PCR) array. The EROD median effect concentration (EC50) values were lower for extracts with greater organohalogen contaminant burdens and thus permitted an initial ranking of colonies based on the efficacy of eliciting an aryl hydrocarbon receptor–mediated response. The ToxChip PCR array data provided a more exhaustive, pathway‐based evaluation of extract effects; variability in the transcriptomic profiles was associated with organohalogen contaminant burdens. For example, extracts from Mud Island (Detroit River, MI, USA) had among the highest organohalogen contaminant burdens and elicited a greater biochemical (EROD EC50 = 0.005) and transcriptomic response (22/43 genes altered on the array) in CEHs compared with the least contaminated site, which was Mandarte Island (BC, Canada; EROD EC50 = 0.172; 8/43 genes altered). Avian eggs represent a useful biomonitoring tool for determining complex mixture effects, and the combination of a rapid extraction method, an in vitro bioassay, and targeted endpoint evaluation (biochemical and transcriptomic) shows great promise as an environmental effects monitoring approach. Environ Toxicol Chem 2019;38:811–819. © 2019 Crown in the right of Canada. Published by Wiley Periodicals Inc. on behalf of SETAC.

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Cytochrome P450 1B1: An unexpected modulator of liver fatty acid homeostasis

Cited by 46 publications

References 96 publications

Diet-dependent retinoid effects on liver gene expression include stellate and inflammation markers and parallel effects of the nuclear repressor Shp

Diet-dependent retinoid effects on liver gene expression include stellate and inflammation markers and parallel effects of the nuclear repressor Shp

Cytochrome P450 Cyp1b1*2 Gene and Its Association With T2d in Tabuk Population, Northwestern Region of Saudi Arabia

A rapid method of preparing complex organohalogen extracts from avian eggs: Applications to in vitro toxicogenomics screening

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