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  1. Article ; Online: Ketogenic diet administration to mice after a high-fat-diet regimen promotes weight loss, glycemic normalization and induces adaptations of ketogenic pathways in liver and kidney

    Souad Nasser / Thomas Solé / Nathalie Vega / Thierry Thomas / Aneta Balcerczyk / Maura Strigini / Luciano Pirola

    Molecular Metabolism, Vol 65, Iss , Pp 101578- (2022)

    2022  

    Abstract: Objective: The ketogenic diet (KD), characterized by very limited dietary carbohydrate intake and used as nutritional treatment for GLUT1-deficiency syndromes and pharmacologically refractory epilepsy, may promote weight loss and improve metabolic ... ...

    Abstract Objective: The ketogenic diet (KD), characterized by very limited dietary carbohydrate intake and used as nutritional treatment for GLUT1-deficiency syndromes and pharmacologically refractory epilepsy, may promote weight loss and improve metabolic fitness, potentially alleviating the symptoms of osteoarthritis. Here, we have studied the effects of administration of a ketogenic diet in mice previously rendered obese by feeding a high fat diet (HFD) and submitted to surgical destabilization of the medial meniscus to mimic osteoarthritis. Methods: 6-weeks old mice were fed an HFD for 10 weeks and then switched to a chow diet (CD), KD or maintained on a HFD for 8 weeks. Glycemia, β-hydroxybutyrate (BHB), body weight and fat mass were compared among groups. In liver and kidney, protein expression and histone post-translational modifications were assessed by Western blot, and gene expression by quantitative Real-Time PCR. Results: After a 10 weeks HDF feeding, administration for 8 weeks of a KD or CD induced a comparable weight loss and decrease in fat mass, with better glycemic normalization in the KD group. Histone β-hydroxybutyrylation, but not histone acetylation, was increased in the liver and kidney of mice fed the KD and the rate-limiting ketogenic enzyme HMGCS2 was upregulated – at the gene and protein level – in liver and, to an even greater extent, in kidney. KD-induced HMGCS2 overexpression may be dependent on FGF21, whose gene expression was increased by KD in liver. Conclusions: Over a period of 8 weeks, KD is more effective than a chow diet to induce metabolic normalization. Besides acting as a fuel molecule, BHB may exert its metabolic effects through modulation of the epigenome - via histone β-hydroxybutyrylation - and extensive transcriptional modulation in liver and kidney.
    Keywords Ketogenesis ; Ketogenic diet ; β-hydroxybutyrate ; Histone PTMs ; HMGCS2 ; Internal medicine ; RC31-1245
    Subject code 570
    Language English
    Publishing date 2022-11-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Impact of Estrogen Withdrawal and Replacement in Female Mice along the Intestinal Tract. Comparison of E2 Replacement with the Effect of a Mixture of Low Dose Pollutants

    Claudie Pinteur / Benoit Julien / Nathalie Véga / Hubert Vidal / Danielle Naville / Brigitte Le Magueresse-Battistoni

    International Journal of Environmental Research and Public Health, Vol 18, Iss 8685, p

    2021  Volume 8685

    Abstract: Postmenopausal women represent a vulnerable population towards endocrine disruptors due to hormonal deficit. We previously demonstrated that chronic exposure of ovariectomized C57Bl6/J mice fed a high-fat, high-sucrose diet to a low-dose mixture of ... ...

    Abstract Postmenopausal women represent a vulnerable population towards endocrine disruptors due to hormonal deficit. We previously demonstrated that chronic exposure of ovariectomized C57Bl6/J mice fed a high-fat, high-sucrose diet to a low-dose mixture of chemicals with one dioxin, one polychlorobiphenyl, one phthalate, and bisphenol A triggered metabolic alterations in the liver but the intestine was not explored. Yet, the gastrointestinal tract is the main route by which pollutants enter the body. In the present study, we investigated the metabolic consequences of ovarian withdrawal and E2 replacement on the various gut segments along with investigating the impact of the mixture of pollutants. We showed that genes encoding estrogen receptors (Esr1, Gper1 not Esr2), xenobiotic processing genes (e.g., Cyp3a11, Cyp2b10), and genes related to gut homeostasis in the jejunum (e.g., Cd36, Got2, Mmp7) and to bile acid biosynthesis in the gut (e.g., Fgf15, Slc10a2) and liver (e.g., Abcb11, Slc10a1) were under estrogen regulation. Exposure to pollutants mimicked some of the effects of E2 replacement, particularly in the ileum (e.g., Esr1, Nr1c1) suggesting that the mixture had estrogen-mimetic activities. The present findings have important implications for the understanding of estrogen-dependent metabolic alterations with regards to situations of loss of estrogens as observed after menopause.
    Keywords ovariectomy ; estradiol replacement ; gut-liver tissue axis ; high-fat ; high-sucrose diet ; mixture of pollutants ; metabolic disorders ; Medicine ; R
    Subject code 570
    Language English
    Publishing date 2021-08-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Gene Network Analysis of Glucose Linked Signaling Pathways and Their Role in Human Hepatocellular Carcinoma Cell Growth and Survival in HuH7 and HepG2 Cell Lines

    Emmanuelle Berger / Nathalie Vega / Michèle Weiss-Gayet / Alain Géloën

    BioMed Research International, Vol

    2015  Volume 2015

    Abstract: Cancer progression may be affected by metabolism. In this study, we aimed to analyze the effect of glucose on the proliferation and/or survival of human hepatocellular carcinoma (HCC) cells. Human gene datasets regulated by glucose were compared to gene ... ...

    Abstract Cancer progression may be affected by metabolism. In this study, we aimed to analyze the effect of glucose on the proliferation and/or survival of human hepatocellular carcinoma (HCC) cells. Human gene datasets regulated by glucose were compared to gene datasets either dysregulated in HCC or regulated by other signaling pathways. Significant numbers of common genes suggested putative involvement in transcriptional regulations by glucose. Real-time proliferation assays using high (4.5 g/L) versus low (1 g/L) glucose on two human HCC cell lines and specific inhibitors of selected pathways were used for experimental validations. High glucose promoted HuH7 cell proliferation but not that of HepG2 cell line. Gene network analyses suggest that gene transcription by glucose could be mediated at 92% through ChREBP in HepG2 cells, compared to 40% in either other human cells or rodent healthy liver, with alteration of LKB1 (serine/threonine kinase 11) and NOX (NADPH oxidases) signaling pathways and loss of transcriptional regulation of PPARGC1A (peroxisome-proliferator activated receptors gamma coactivator 1) target genes by high glucose. Both PPARA and PPARGC1A regulate transcription of genes commonly regulated by glycolysis, by the antidiabetic agent metformin and by NOX, suggesting their major interplay in the control of HCC progression.
    Keywords Medicine ; R
    Subject code 570
    Language English
    Publishing date 2015-01-01T00:00:00Z
    Publisher Hindawi Limited
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article: Chronic exposure to a pollutant mixture at low doses led to tissue-specific metabolic alterations in male mice fed standard and high-fat high-sucrose diet

    Naville, Danielle / Benoit Julien / Brigitte Le Magueresse-Battistoni / Claudie Pinteur / Guillain Gaillard / Hubert Vidal / Nathalie Vega / Stéphanie Chanon

    Chemosphere. 2019 Apr., v. 220

    2019  

    Abstract: Excessive consumption of industrialized food and beverages is a major etiologic factor in the epidemics of obesity and associated metabolic diseases because these products are rich in fat and sugar. In addition, they contain food contact materials and ... ...

    Abstract Excessive consumption of industrialized food and beverages is a major etiologic factor in the epidemics of obesity and associated metabolic diseases because these products are rich in fat and sugar. In addition, they contain food contact materials and environmental pollutants identified as metabolism disrupting chemicals. To evaluate the metabolic impact of these dietary threats (individually or combined), we used a male mouse model of chronic exposure to a mixture of low-dose archetypal food-contaminating chemicals that was added in standard or high-fat, high-sucrose (HFHS) diet. Specifically, the mixture contained bisphenol A, diethylhexylphthalate, 2,3,7,8-tetrachlorodibenzo-p-dioxine and polychlorinated biphenyl 153. Exposure lasted from 5 to 20 weeks of age. Metabolic exploration was conducted setting the basis of candidate gene expression mRNA analyses in liver, jejunum and adipose tissue depots from 20 week-old mice. Strong metabolic deleterious effects of the HFHS diet were demonstrated in line with obesity-associated metabolic features and insulin resistance. Pollutant exposure resulted in significant changes on plasma triglyceride levels and on the expression levels of genes mainly encoding xenobiotic processing in jejunum; estrogen receptors, regulators of lipoprotein lipase and inflammatory markers in jejunum and adipose tissues as well as adipogenesis markers. Importantly, the impact of pollutants was principally evidenced under standard diet. In addition, depending on nutritional conditions and on the metabolic tissue considered, the impact of pollutants could mimic or oppose the HFHS effects. Collectively, the present study extends the cocktail effect concept of a low-dosed pollutant mixture and originally points to tissue-specificity responsiveness especially in jejunum and adipose tissues.
    Keywords adipogenesis ; adipose tissue ; animal models ; beverages ; bisphenol A ; chronic exposure ; disease outbreaks ; estrogen receptors ; etiology ; food contact surfaces ; gene expression ; genes ; high carbohydrate diet ; industrialization ; insulin resistance ; jejunum ; lipoprotein lipase ; liver ; males ; messenger RNA ; metabolic diseases ; metabolism ; mice ; obesity ; pollutants ; polychlorinated biphenyls ; sugars ; triacylglycerols ; xenobiotics
    Language English
    Dates of publication 2019-04
    Size p. 1187-1199.
    Publishing place Elsevier Ltd
    Document type Article
    ZDB-ID 120089-6
    ISSN 1879-1298 ; 0045-6535 ; 0366-7111
    ISSN (online) 1879-1298
    ISSN 0045-6535 ; 0366-7111
    DOI 10.1016/j.chemosphere.2018.12.177
    Database NAL-Catalogue (AGRICOLA)

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  5. Article ; Online: Metabolic outcome of female mice exposed to a mixture of low-dose pollutants in a diet-induced obesity model.

    Danielle Naville / Emmanuel Labaronne / Nathalie Vega / Claudie Pinteur / Emmanuelle Canet-Soulas / Hubert Vidal / Brigitte Le Magueresse-Battistoni

    PLoS ONE, Vol 10, Iss 4, p e

    2015  Volume 0124015

    Abstract: Pollutants are suspected to contribute to the etiology of obesity and related metabolic disorders. Apart from occupational exposure which concerns a subset of chemicals, humans are mostly exposed to a large variety of chemicals, all life-long and at low ... ...

    Abstract Pollutants are suspected to contribute to the etiology of obesity and related metabolic disorders. Apart from occupational exposure which concerns a subset of chemicals, humans are mostly exposed to a large variety of chemicals, all life-long and at low doses. Food ingestion is a major route of exposure and it is suggested that pollutants have a worsened impact when combined with a high-fat diet. In the experimental studies described herein, we aimed to add further evidence on the metabolic impact of food pollutants using a recently set up model in which mice are life-long fed a high-fat/high-sucrose diet (HFSD) with/without common food pollutants shown to exhibit metabolic disrupting activities. Specifically, this mixture comprised bisphenol A, dioxin, polychlorobiphenyl PCB153, and phthalate and was added in HFSD at doses resulting in mice exposure at the Tolerable Daily Intake dose range for each pollutant. We herein focused on the 7-week-old females which exhibited early signs of obesity upon HFSD feeding. We observed no signs of toxicity and no additional weight gain following exposure to the mixture but alleviated HFSD-induced glucose intolerance in the absence of alteration of gluconeogenesis and steatosis. It suggested that the observed metabolic improvement was more likely due to effects on muscle and/or adipose tissues rather than on the liver. Consistently, female mice exhibited enhanced lean/fat mass ratio and skeletal muscle insulin sensitivity. Moreover, expression levels of inflammatory markers were reduced in adipose tissue at 7 but enhanced at 12 weeks of age in agreement with the inverse alterations of glucose tolerance observed at these ages upon pollutant exposure in the HFSD-fed females. Collectively, these data suggest apparent biphasic effects of pollutants upon HFSD feeding along with obesity development. These effects were not observed in males and may depend on interactions between diet and pollutants.
    Keywords Medicine ; R ; Science ; Q
    Subject code 590
    Language English
    Publishing date 2015-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article: Low-dose pollutant mixture triggers metabolic disturbances in female mice leading to common and specific features as compared to a high-fat diet

    Labaronne, Emmanuel / Benoit Julien / Brigitte Le Magueresse-Battistoni / Claudie Pinteur / Danielle Naville / Emmanuelle Meugnier-Fouilloux / Hubert Vidal / Nathalie Vega / Sandra Pesenti

    Journal of nutritional biochemistry. 2017 July, v. 45

    2017  

    Abstract: Environmental pollutants are potential etiologic factors of obesity and diabetes that reach epidemic proportions worldwide. However, it is important to determine if pollutants could exert metabolic defects without directly inducing obesity. The metabolic ...

    Abstract Environmental pollutants are potential etiologic factors of obesity and diabetes that reach epidemic proportions worldwide. However, it is important to determine if pollutants could exert metabolic defects without directly inducing obesity. The metabolic disturbances triggered in nonobese mice lifelong exposed to a mixture of low-dose pollutants (2,3,7,8-tetrachlorodibenzo-p-dioxine, polychlorinated biphenyl 153, diethylhexyl-phthalate, and bisphenol A) were compared with changes provoked by a high-fat high-sucrose (HFHS) diet not containing the pollutant mixture. Interestingly, females exposed to pollutants exhibited modifications in lipid homeostasis including a significant increase of hepatic triglycerides but also distinct features from those observed in diet-induced obese mice. For example, they did not gain weight nor was glucose tolerance impacted. To get more insight, a transcriptomic analysis was performed in liver for comparison. We observed that in addition to the xenobiotic/drug metabolism pathway, analysis of the hepatic signature illustrated that the steroid/cholesterol, fatty acid/lipid and circadian clock metabolic pathways were targeted in response to pollutants as observed in the diet-induced obese mice. However, the specific sets of dysregulated annotated genes (>1300) did not overlap more than 40% between both challenges with some genes specifically altered only in response to pollutant exposure. Collectively, results show that pollutants and HFHS affect common metabolic pathways, but by different, albeit overlapping, mechanisms. This is highly relevant for understanding the synergistic effects between pollutants and the obesogenic diet reported in the literature.
    Keywords animal disease models ; biochemical pathways ; bisphenol A ; cholesterol ; circadian rhythm ; diabetes ; etiology ; fatty acids ; females ; genes ; glucose tolerance ; high fat diet ; homeostasis ; liver ; mice ; obesity ; obesogenic diet ; pharmacokinetics ; pollutants ; polychlorinated biphenyls ; synergism ; transcriptomics ; triacylglycerols ; xenobiotics
    Language English
    Dates of publication 2017-07
    Size p. 83-93.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 1014929-6
    ISSN 1873-4847 ; 0955-2863
    ISSN (online) 1873-4847
    ISSN 0955-2863
    DOI 10.1016/j.jnutbio.2017.04.001
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    In stock of ZB MED Bonn / Germany

    Z 5044: Show issues

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