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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE98845 | GEO | 2017/09/26

SECONDARY ACCESSION(S): PRJNA386385

REPOSITORIES: GEO

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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

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

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

2011-06-01 | GSE27271 | GEO

β-carotene conversion to vitamin A delays atherosclerosis progression by decreasing hepatic lipid secretion in mice

Project description:Atherosclerosis is characterized by the pathological accumulation of cholesterol-laden macrophages in the arterial wall. Atherosclerosis is also the main underlying cause of cardiovascular diseases (CVDs), and its development is largely driven by elevated plasma cholesterol. Strong epidemiological data find an inverse association between plasma β-carotene with atherosclerosis, and we recently showed that β-carotene oxygenase 1 (BCO1) activity, responsible for β-carotene cleavage to vitamin A, is associated with reduced plasma cholesterol in humans and mice. In this study, we explore whether intact β-carotene or vitamin A affect atherosclerosis progression in the atheroprone low-density lipoprotein receptor (LDLR) - deficient mice. In comparison to control-fed Ldlr-/- mice, β-carotene-supplemented mice showed reduced atherosclerotic lesion size at the level of the aortic root and plasma cholesterol levels (P = 0.0003). These changes were absent in Ldlr-/-/Bco1-/- mice, despite accumulating β-carotene in plasma and atherosclerotic lesions. We discarded the implication of myeloid BCO1 in the development of atherosclerosis by performing bone marrow transplant experiments. Lipid production assays found that retinoic acid, the active form of vitamin A, reduced the secretion of newly synthetized triglyceride and cholesteryl ester in cell culture and mice. Overall, our findings provide insights into the role of BCO1 activity and vitamin A in atherosclerosis progression through the regulation of hepatic lipid metabolism.

2020-11-12 | GSE157972 | GEO

Molecular characterisation of High Beta Carotene (HBC) Mutant

Project description:The High-β-Carotene (HBC) mutant identified from EMS mutagenized population of cultivar Arka Vikas and the biochemical studies revealed that mutant fruits contain four times higher level of β-Carotene in comparison to Wild type (cv. Arka Vikas). We have developed whole genome microarray expression profiling as a discovery platform to identify differentially expressed genes in fruits containing High-β-Carotene mutant in comparison to Wild type (cv. Arka Vikas). Tomato fruit tissue samples from different stages of fruit ripening like Mature green, Breaker, Turning and Ripening stages of High-β-Carotene (HBC) mutant and Wild type (cv. Arka VIkas) were used for microarray gene expression analysis. Carotenoid pathway analysis of both mutant and wild type reveals that the high expression of chromoplast specific lycopene- β-cyclase gene in the HBC mutant, which is involved in the conversion of lycopene to β-carotene, but in wild type the expression of this gene, was low. Four genes (PSY, PDS, CRTISO, CYCB) of the carotenoid pathway was quantified in the same RNA samples by real-time PCR, confirming that the variation of the gene expression in HBC mutant.

2017-12-01 | GSE90964 | GEO

Protein expression in beta-carotene transgenic soybeans

Project description:Soybeans (Glycine max) were genetically modified using a gene gun to produce beta-carotene, which is not normally found in the species. beta-carotene is produced in the chloroplast in which it competes with chlorophyl for production. A proteomics analysis was performed to determine the effects of the transgene on seed protein content.

2016-07-19 | PXD000709 | Pride

Excess folic acid supplementation increases adiposity and impacts insulin sensitivity in female mice during pregnancy and has sex-specific effects on fetal offspring

Project description:We determined the effects of excess folic acid supplementation (5x recommendation) on maternal and fetal offspring metabolic health. Using a mouse (female C57BL/6J) model of gestational dibetes (GDM; 45% kcal fat diet) and control mice (10% kcal diet) we show that folic acid supplementation increased weight gain and fat mass in both GDM and control mice but improved insulin sensitivity in GDM mice and worsened insulin sensitivity in control mice. We found no unmetabolized folic acid in liver from supplemented mice suggesting the metabolic effects of folic acid supplementation may not be due to unmetabolized folic acid. Male fetal (gestational day 18.5) offspring from folic acid supplemented dams (GDM and control) had greater beta cell mass and density than those from unsupplemented dams; this was not observed in female offspring. Differential sex-specific hepatic gene expression profiles were observed in the offspring from supplemented dams but this differed between GDM and controls. Our findings suggest that folic acid supplementation affects insulin sensitivity in female mice, but is dependent on their metabolic phenotype, and has sex-specific effects on offspring pancreas and liver.

2023-09-29 | GSE237149 | GEO

Transcriptomic characterization of the impact of 2'-fucosyllactose supplementation on intestinal adaptation following ileocecal resection.

Project description:Purpose: To identify the impact of 2'-FL supplementation on adaptive response following extensive intestinal resection. Methods: Transcriptomic profiles were obtained from mice undergoing ileocecal recection (8-10 week old male mice) and again at 8 weeks post-surgery. At the time of resection and again at 8 weeks post-op, small bowel samples were obtained from treatment and control animals and submitted for mRNA profiling. During these 8 weeks treatment animals (n=3) received 2'-FL supplementationion while controls (n=3) received only standard diet. Results: We observe enrichment in genes and pathways related to anti-microbial peptides, metabolism, and energy processing. Supplementation of 2'-FL increases energy availability and enhances the adaptive response. Male C57BL/6 mice at 8 to 10 weeks of age were submitted to ileocecal recection. Following resection, half were supplemented with 2'-FL for 8 weeks; small bowels were obtained and submitted for mRNA profiling,

2016-04-01 | E-GEOD-72590 | biostudies-arrayexpress

mRNA array in liver tissue samples of Sprague-Dawley rats

Project description:Non-alcoholic fatty liver disease (NAFLD) has increased over the last decades and may evolve into hepatocellular carcinoma (HCC). As HCC is challenging to treat, knowledge on the modifia-ble risk factors for NAFLD/HCC, (e.g. hypercaloric diets rich in fructose) is essential. We used a model of diethyl nitrosamine-induced hepatocarcinogenesis to investigate the liver cancer-promoting effects of a diet supplemented with 10% liquid fructose, administered to male and female rats for 11 months. A subset of the fructose-supplemented rats received resveratrol in the last 4 months of treatment. We observed metabolic abnormalities mainly in the female fructose-supplemented rats (increases in weight, adiposity, and plasma glucose and triglycerides, as well as liver triglycerides and a reduced insulin sensitivity index), which were partially reversed by resveratrol. The livers of fructose-supplemented rats showed no de visu or histological evi-dence of liver tumorigenesis. Targeted analysis of 84 cancer-related genes in the female liver samples revealed expression changes associated with cancer-related pathways, but individual genes indicated that some changes increased the risk of hepatocarcinogenesis (Sfrp2, Ccl5, Socs3, and Gstp1), while others exerted a protective/preventive effect (Bcl2 and Cdh1). In conclusion, our data do not clearly demonstrate that chronic fructose supplementation promotes HCC development in rats.

2020-12-30 | GSE163966 | GEO

A folic acid-enriched diet attenuates prostate involution in response to androgen deprivation

Project description:Folic acid is present in pre-natal vitamins, fortified cereal grains and multi-vitamin supplements. High intake of folic acid through these sources has resulted in populations with increased levels of serum folate and unmetabolized folic acid. Although the benefits of folic acid in the prevention of neural tube defects are undeniable, the impact of long-term consumption of folic acid on the prostate is not fully understood. In this study, we used a rodent model to test whether dietary folic acid (FA) supplementation changes prostate homeostasis and response to androgen deprivation. Although intact prostate weights do not differ between diet groups, we made the surprising observation that dietary folic acid supplementation confers partial resistance to castration-mediated prostate involution. More specifically, male mice that were fed a folic acid supplemented diet and then castrated had greater prostate wet weights, greater prostatic luminal epithelial cell heights, and more abundant RNAs encoding prostate secretory proteins compared to mice that were fed a control diet and castrated. We used RNA-seq to identify signaling pathways enriched in the castrated prostates from folic acid supplemented diet fed mice compared to control mice. We observed differential expression of genes involved in several metabolic pathways in the FA supplemented mice. Together, our results show that dietary FA supplementation can impact metabolism in the prostate and attenuate the prostate’s response to androgen deprivation. This has important implications for androgen deprivation therapies used in the treatment of prostate disease, as consumption of high levels of folic acid could reduce the efficacy of these treatments.

2018-08-22 | GSE116299 | GEO

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