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Adipose tissue analysis of wild-type and beta-carotene 15-15'-oxygenase 1 (Bcmo1) ko mice fed under control diet and beta-carotene diet

ABSTRACT: Cell culture studies indicate that beta-carotene-(BC)-derived apocarotenoid signaling molecules influence the activities of nuclear receptors that regulate many aspects of adipocyte physiology. Here, we analyzed the roles of the two BC metabolizing enzymes, BCMO1 and BCDO2, for this process in mouse models. Wild-type mice converted BC into retinoids and showed reduced body adiposity (by 28%), leptinemia and adipocyte size. Genome wide microarray analysis revealed a generalized decrease of mRNA expression of peroxisome proliferator-activated receptor gamma (PPARgamma) target genes. Consistently, the expression of this key transcription factor for lipogenesis was significantly reduced both on the mRNA and protein levels. This effect of BC was absent in Bcmo1-/- mice that showed increased BCDO2 expression and gamma-10gamma-apocarotenoid production. Our study evidences an important role of BC for the control of body adiposity in mice and identifies Bcmo1 as critical molecular player for the regulation of PPARgamma activity.

ORGANISM(S): Mus musculus

PROVIDER: GSE27271 | GEO | 2011/06/01

SECONDARY ACCESSION(S): PRJNA137133

REPOSITORIES: GEO

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Adipose tissue analysis of wild-type and beta-carotene 15-15'-oxygenase 1 (Bcmo1) ko mice fed under control diet and beta-carotene diet

Project description:Cell culture studies indicate that beta-carotene-(BC)-derived apocarotenoid signaling molecules influence the activities of nuclear receptors that regulate many aspects of adipocyte physiology. Here, we analyzed the roles of the two BC metabolizing enzymes, BCMO1 and BCDO2, for this process in mouse models. Wild-type mice converted BC into retinoids and showed reduced body adiposity (by 28%), leptinemia and adipocyte size. Genome wide microarray analysis revealed a generalized decrease of mRNA expression of peroxisome proliferator-activated receptor gamma (PPARgamma) target genes. Consistently, the expression of this key transcription factor for lipogenesis was significantly reduced both on the mRNA and protein levels. This effect of BC was absent in Bcmo1-/- mice that showed increased BCDO2 expression and gamma-10gamma-apocarotenoid production. Our study evidences an important role of BC for the control of body adiposity in mice and identifies Bcmo1 as critical molecular player for the regulation of PPARgamma activity. The goal of the study was to analyze the putative differential effects of BC accumulation on Bcmo1 ko mice, and BC metabolites in wt mice. Inguinal adipose tissue gene expression profile comparing adult male and female mice under control diet and beta-carotene (BC) supplemented diet during 14 weeks. 47 mice in total. 23 wild-type (11 male/12 female) and 24 bcmo1 (12 male/12 female) mice, fed on vitamin A diet (1500 IU vit A/kg diet) or vitamin A diet supplemented with BC (1500 IU vit A/kg diet +150 mg BC/kg diet) during 14 weeks.

2011-06-01 | E-GEOD-27271 | biostudies-arrayexpress

Nutritional effects by beta-carotene in lung in males and females of control mice versus BCMO knockout mice

Project description:Molecular mechanisms triggered by high dietary beta-carotene (BC) intake in lung are largely unknown. We performed microarray gene expression analysis on lung tissue of BC supplemented beta-carotene 15,150-monooxygenase 1 knockout (Bcmo1-/-) mice, which are—like humans—able to accumulate BC. Our main observation was that the genes were regulated in an opposite direction in male and female Bcmo1-/- mice by BC. The steroid biosynthetic pathway was overrepresented in BC-supplemented male Bcmo1-/- mice. Testosterone levels were higher after BC supplementation only in Bcmo1-/- mice, which had, unlike wild-type (Bcmo1+/+) mice, large variations. We hypothesize that BC possibly affects hormone synthesis or metabolism. Since sex hormones influence lung cancer risk, these data might contribute to an explanation for the previously found increased lung cancer risk after BC supplementation (ATBC and CARET studies). Moreover, effects of BC may depend on the presence of frequent human BCMO1 polymorphisms, since these effects were not found in wild-type mice.

2017-09-26 | GSE98845 | GEO

Nutritional effects by beta-carotene in liver in males and females of control wildtype mice versus BCMO knockout mice

Project description:Molecular mechanisms triggered by high dietary beta-carotene (BC) intake in liver are largely unknown. We performed microarray gene expression analysis on liver tissue of BC supplemented beta-carotene 15,150-monooxygenase 1 knockout (Bcmo1-/-) mice, which are—like humans—able to accumulate BC. This was compared with litter mates being wild-type (Bcmo1+/+) mice, and we analysed both males and females, as we previously showed that in lung tissue we observed opposite gene regulation between males and females (Van Helden et al., CMLS 2011).

2017-09-26 | GSE98846 | GEO

Biochemical evidence for the tyrosine involvement in cationic intermediate stabilization in mouse beta-carotene 15, 15'-monooxygenase.

Project description: Not available

| S-EPMC2801523 | biostudies-literature

Angiogenesis in Balb/c mice under beta-carotene supplementation in diet.

Project description: Not available

| S-EPMC2820200 | biostudies-literature

ZFP423 Controls EBF2 Co-activator Recruitment and PPARgamma Occupancy to Determine the Thermogenic Plasticity of Adipocytes_ChIP-seq

Project description:Energy-storing white adipocytes maintain their identity by suppressing the gene program defining energy-burning thermogenic brown/beige adipocytes. Here, we reveal that the protein-protein interaction between the transcriptional co-regulator ZFP423 and brown/beige cell determination factor, EBF2, is essential for restraining the thermogenic phenotype of white adipose tissue (WAT). Disruption of the ZFP423-EBF2 protein interaction through CRISPR-Cas9 gene editing triggers widespread “browning” of WAT in adult mice. Mechanistically, adipocyte Zfp423 deficiency induces an EBF2 NuRD-to-BAF co-regulator switch and a shift in PPARgamma occupancy to thermogenic genes. This shift in PPARgamma occupancy increases the anti-diabetic efficacy of the PPARgamma agonist rosiglitazone in obesity while diminishing the unwanted weight-gaining effect of the drug. These data indicate that ZFP423 controls EBF2 co-activator recruitment and PPARgamma occupancy to determine the thermogenic plasticity of adipocytes and raise the concept of targeting transcriptional brakes in adipocyte gene expression as a therapeutic strategy to induce thermogenic adipocyte biogenesis in obesity.

2022-05-01 | GSE175654 | GEO

ZFP423 Controls EBF2 Co-activator Recruitment and PPARgamma Occupancy to Determine the Thermogenic Plasticity of Adipocytes_ChAP-seq

2022-05-01 | GSE175653 | GEO

Transcriptional analysis of PPARgamma activation in control and PPARgamma null macrophages [ChIP-seq]

Project description:The nuclear receptor Peroxisome Proliferator Activated Receptor gamma (PPARgamma) is known to regulate lipid metabolism in many tissues, including macrophages. Here we report that macrophage respiration is enhanced by rosiglitazone, an activating PPARgamma ligand, in a PPARgamma dependent manner. Moreover, PPARgamma is required for macrophage respiration even in the absence of exogenous ligand. Unexpectedly, the absence of PPARgamma dramatically affects the oxidation of glutamine. Both glutamine and PPARgamma have been implicated in alternative activation (AA) of macrophages and PPARgamma was required for IL4-dependent gene expression and stimulation of macrophage respiration. Remarkably, depletion of PPARgamma phenocopied the effects of glutamine depletion on transcription. Thus, PPARgamma supports alternative activation by facilitating glutamine metabolism. Yet PPARgamma expression is itself markedly increased by IL4. Thus, PPARgamma functions at the center of a feed forward loop that is central to AA of macrophages.

2018-09-06 | GSE111104 | GEO

Transcriptional analysis of PPARgamma activation in control and PPARgamma null macrophages [GRO-seq]

2018-09-06 | GSE111103 | GEO

Transcriptional analysis of PPARgamma activation in control and PPARgamma null macrophages [RNA-seq]

2018-09-06 | GSE111102 | GEO