Jean-Marc A Lobaccaro

Université Blaise Pascal - Clermont-Ferrand II, Clermont, Auvergne, France

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Publications (70)329.52 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Enolase is a glycolytic enzyme known to inhibit cholesteryl ester hydrolases (CEHs). Cholesteryl ester loading of macrophages, as occurs during atherosclerosis, is accompanied by increased Enolase protein and activity. Here, we describe that J774 macrophages treated with LXR agonists exhibit reduced Enolase transcript and protein abundance. Moreover, we show that this reduction is further potentiated by activation of the LXR/RXR heterodimer with the RXR ligand 9-cis retinoic acid. Enolase levels are also reduced in vivo following activation of LXRs in the intestine, but not in the liver. This effect is lost in Lxrαβ-/- mice. In aggregate, our study identified Enolase as a new target of LXRs in vivo, which may promote cholesterol mobilization for subsequent efflux. Copyright © 2015. Published by Elsevier Inc.
    Steroids 02/2015; 99. DOI:10.1016/j.steroids.2015.02.010 · 2.72 Impact Factor
  • Anthony Alioui, Olivier Celhay, Silvère Baron, Jean-Marc A Lobaccaro
    Clinical Lipidology 12/2014; 9(6):643-655. DOI:10.2217/clp.14.51 · 0.86 Impact Factor
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    ABSTRACT: Essential oils are widely used in pharmaceutical, sanitary, cosmetic, agriculture and food industries for their bactericidal, virucidal, fungicidal, antiparasitical and insecticidal properties. Their anticancer activity is well documented. Over a hundred essential oils from more than twenty plant families have been tested on more than twenty types of cancers in last past ten years. This review is focused on the activity of essential oils and their com-ponents on various types of cancers. For some of them the mechanisms involved in their anticancer activities have been carried out. Introduction Recognized since ancient times for their medic-inal value, but often considered as a relic of medieval medical practice by representatives of modern medicine, essential oils (EOs) are currently receiving therapeutic interest fully renewed. Thus, during recent years, plant EOs have come more into the focus of phytomedi-cine [1, 2]. Their widespread use has raised the interest of scientists in basic research of EOs. Especially, anti-microbial and anti-oxidant activities as well as potential anti-cancer activ-ity have been investigated in recent years [3, 4]. Cancer is the second largest single cause of death claiming over six million lives every year worldwide [5]. There has been a recent upsurge in the use of natural products to supersede cur-rent treatment in patients that develop multi-drug resistance. Scientific studies of plants used in various types of ethnic medicine has led to the discovery of many valuable drugs, including taxol, camptothecin, vincristine and vinblastine [6, 7]. Many studies pointed out anticancer properties of other plants [8-11]. Over five hundred papers have been published on anticancer activity of EOs. The first publica-tions on the anticancer activity of essential oils dated to 1960s. So far, the effects of EOs have been investigated on glioblastoma, melanoma, leukemia and oral cancers, as well as on bone, breast, cervix, colon, kidney, liver, lung, ovary, pancreas, prostate, and uterus cancers. The aim of this review is to state the work car-ried out on the anticancer properties of EOs, their mode of action and the types of cancers targeted.
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    ABSTRACT: The small heterodimer partner (NR0B2) is an atypical nuclear receptor known mainly for its role in bile acid homeostasis in the enterohepatic tract. We previously showed that NR0B2 controls testicular functions such as testosterone synthesis. Moreover, NR0B2 mediates the deleterious testicular effects of estrogenic endocrine disruptors leading to infertility. The endocrine homeostasis is essential for health as it controls many physiological functions. This is supported by a large number of studies demonstrating that alterations of steroid activity lead to several kinds of diseases such as obesity and infertility. Within the testis, the functions of the Leydig cells are mainly controlled by the hypothalamo-pituitary (HP) axis via luteinizing hormone/chorionic gonadotropin (LH/CG). Here we show that LH/CG represses Nr0b2 expression through the PKA-AMPK pathway. Moreover, using a transgenic mouse model invalidated for Nr0b2, we point out that NR0B2 mediates the repression of testosterone synthesis and subsequent germ cell apoptosis induced by exposure to anti-GnRH compound. Together, our data demonstrate a new link between HP axis and NR0B2 in testicular androgen metabolism, making NR0B2 a major actor of testicular physiology in case of alteration of LH/CG levels.
    Endocrinology 11/2014; 156(2):en20141418. DOI:10.1210/en.2014-1418 · 4.64 Impact Factor
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    ABSTRACT: Objective: To determine whether the transcription factors liver X receptors (LXRs) and their downstream genes, which are involved in the regulation of several testicular functions in mouse models, are differentially expressed in testes of men with nonobstructive azoospermia (NOA) or obstructive azoospermia (OA). Design: Prospective study. Setting: University hospital. Patient(s): Patients with various types of NOA (n = 22) and with OA (n = 5). Intervention(s): Human testicular biopsies. Main Outcome Measure(s): Transcript levels were measured in testicular biopsies with the use of quantitative polymerase chain reaction. Correlations of LXR mRNA levels with the number of germ cells, the expression of proliferation and apoptosis markers, and the amount of intratesticular lipids and testosterone were evaluated. The localization of LXR alpha was analyzed by immunofluorescence. Result(s): LXR mRNA levels were decreased by 49%-98% in NOA specimens and positively correlated with germ cell number. Accumulations of IDOL and SREBP1c (LXR targets involved in lipid homeostasis) were 1.8-2.1 times lower in NOA samples and mRNA levels of the SREBP1c target gene ELOVL6 were increased 1.9-2.4-fold. Interestingly, the amount of triglycerides and free fatty acids were higher in NOA testes (3.4-12.2-fold). LXR alpha was present in Leydig cells. Accumulations of LXR downstream genes encoding the steroidogenic proteins StAR and 3 beta HSD2 were higher in NOA testes (5.9-12.8-fold). Conclusion(s): Knowledge of changes in the transcript levels of LXRs and some of their downstream genes during altered spermatogenesis may help us to better understand the physiopathology of testicular failure in azoospermic patients. ((C)2014 by American Society for Reproductive Medicine.)
    Fertility and Sterility 05/2014; 102(2). DOI:10.1016/j.fertnstert.2014.04.033 · 4.59 Impact Factor
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    ABSTRACT: This research highlights the chemical composition, antioxidant, anti-inflammatory and anti-proliferative activities of essential oils from leaves of Ocimum basilicum, Ocimum americanum, Hyptis spicigera, Lippia multiflora, Ageratum conyzoides, Eucalyptus camaldulensis and Zingiber officinale. Essential oils were analyzed by gas chromatography-mass spectrometry and gas chromatography-flame ionization detector. Major constituents were α-terpineol (59.78%) and β-caryophyllene (10.54%) for Ocimum basilicum; 1, 8-cineol (31.22%), camphor (12.730%), α-pinene (6.87%) and trans α-bergamotene (5.32%) for Ocimum americanum; β-caryophyllene (21%), α-pinene (20.11%), sabinene (10.26%), β-pinene (9.22%) and α-phellandrene (7.03%) for Hyptis spicigera; p-cymene (25.27%), β-caryophyllene (12.70%), thymol (11.88), γ-terpinene (9.17%) and thymyle acetate (7.64%) for Lippia multiflora; precocene (82.10%)for Ageratum conyzoides; eucalyptol (59.55%), α-pinene (9.17%) and limonene (8.76%) for Eucalyptus camaldulensis; arcurcumene (16.67%), camphene (12.70%), zingiberene (8.40%), β-bisabolene (7.83%) and β-sesquiphellandrène (5.34%) for Zingiber officinale. Antioxidant activities were examined using 1,1-diphenyl-2-picryl-hydrazyl (DPPH) and 2,2'-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid (ABTS) methods. O. basilicum and L. multiflora exhibited the highest antioxidant activity in DPPH and ABTS tests, respectively. Anti-inflammatory properties were evaluated by measuring the inhibition of lipoxygenase activity and essential oil of Z. officinale was the most active. Anti-proliferative effect was assayed by the measurement of MTT on LNCaP and PC-3 prostate cancer cell lines, and SF-763 and SF-767 glioblastoma cell lines. Essential oils from A. conyzoides and L. multiflora were the most active on LNCaP and PC-3 cell lines, respectively. The SF-767 glioblastoma cell line was the most sensitive to O. basilicum and L. multiflora EOs while essential oil of A. conyzoides showed the highest activity on SF-763 cells. Altogether these results justify the use of these plants in traditional medicine in Burkina Faso and open a new field of investigation in the characterization of the molecules involved in anti-proliferative processes.
    PLoS ONE 03/2014; 9(3):e92122. DOI:10.1371/journal.pone.0092122 · 3.53 Impact Factor
  • Jean-Marc A Lobaccaro, Amalia Trousson
    Endocrinology 03/2014; 155(3):656-8. DOI:10.1210/en.2014-1057 · 4.64 Impact Factor
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    ABSTRACT: Liver X Receptors LXRα (NR1H3) and LXRβ (NR1H2) are transcription factors belonging to the nuclear receptor superfamily, activated by specific oxysterols, oxidized derivatives of cholesterol. These receptors are involved in the regulation of testis physiology. Lxr-deficient mice pointed to the physiological roles of these nuclear receptors in steroid synthesis, lipid homeostasis and germ cell apoptosis and proliferation. Diethylstilbestrol (DES) is a synthetic estrogen considered as an endocrine disruptor that affects the functions of the testis. Various lines of evidences have made a clear link between estrogens, their nuclear receptors ERα (NR3A1) and ERβ (NR3A2), and Lxrα/β. As LXR activity could also be regulated by the nuclear receptor small heterodimer partner (SHP, NR0A2) and DES could act through SHP, we wondered whether LXR could be targeted by estrogen-like endocrine disruptors such as DES. For that purpose, wild-type and Lxr-deficient mice were daily treated with 0.75 μg DES from day 1 to 5 after birth. The effects of DES were investigated at 10 or 45 days of age. We demonstrated that DES induced a decrease of the body mass at 10 days only in the Lxr-deficient mice suggesting a protective effect of Lxr. We defined three categories of DES-target genes in testis: those whose accumulation is independent of Lxr; those whose accumulation is enhanced by the lack of both Lxrα/β; those whose accumulation is repressed by the absence of Lxrα/β. Lipid accumulation is also modified by neonatal DES injection. Lxr-deficient mice present different lipid profiles, demonstrating that DES could have its effects in part due to Lxrα/β. Altogether, our study shows that both nuclear receptors Lxrα and Lxrβ are not only basally important for testicular physiology but could also have a preventive effect against estrogen-like endocrine disruptors.
    Biochemical and Biophysical Research Communications 12/2013; 446(3). DOI:10.1016/j.bbrc.2013.12.005 · 2.28 Impact Factor
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    ABSTRACT: Introduction: Oxysterols are implicated in various cellular processes. Among their target proteins, liver X receptors (LXRs) α and β modulate the cell cycle in a large range of cancer cell lines. Besides their role as cholesterol sensors, LXRs are also involved in the proliferation/apoptosis balance regulation in various types of cancers. Areas covered: This review covers oxysterols and derivatives of cholesterol as well as synthetic or natural ligands (agonist/antagonist) of LXRs. Most tumor cell lines are sensitive to LXR activation. Indeed various cancers are concerned such as prostate, breast, glioblastoma, colorectal, and ovary tumors, and leukemia. Expert opinion: Developing the use of LXR ligands in human health, especially in the field of cancer, represents a novel and promising strategy. Despite a wide spectrum of applications, numerous adverse effects of LXR activation need to be solved before genuine clinical trials in humans. Future directions will be based on the engineering of selective LXRs modulators (SLiMs) as already done for nuclear steroid receptors.
    Expert Opinion on Therapeutic Targets 07/2013; 17(9). DOI:10.1517/14728222.2013.820708 · 4.90 Impact Factor
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    ABSTRACT: Bile acids are cholesterol metabolites that have been extensively studied in recent decades. In addition to having ancestral roles in digestion and fat solubilization, bile acids have recently been described as signaling molecules involved in many physiological functions, such as glucose and energy metabolisms. These signaling pathways involve the activation of the nuclear receptor farnesoid X receptor (FXRα) or of the G protein-coupled receptor TGR5. In this review, we will focus on the emerging role of FXRα, suggesting important functions for the receptor in steroid metabolism. It has been described that FXRα is expressed in the adrenal glands and testes, where it seems to control steroid production. FXRα also participates in steroid catabolism in the liver and interferes with the steroid signaling pathways in target tissues via crosstalk with steroid receptors. In this review, we discuss the potential impacts of bile acid (BA), through its interactions with steroid metabolism, on glucose metabolism, sexual function, and prostate and breast cancers. Although several of the published reports rely on in vitro studies, they highlight the need to understand the interactions that may affect health. This effect is important because BA levels are increased in several pathophysiological conditions related to liver injuries. Additionally, BA receptors are targeted clinically using therapeutics to treat liver diseases, diabetes, and cancers.
    Cellular and Molecular Life Sciences CMLS 06/2013; DOI:10.1007/s00018-013-1387-0 · 5.86 Impact Factor
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    ABSTRACT: LXR (Liver X Receptors) act as "sensor" proteins that regulate cholesterol uptake, storage, and efflux. LXR signaling is known to influence proliferation of different cell types including human prostatic carcinoma (PCa) cell lines. This study shows that deletion of LXR in mouse fed a high-cholesterol diet recapitulates initial steps of PCa development. Elevation of circulating cholesterol in Lxrαβ-/- double knockout mice results in aberrant cholesterol ester accumulation and prostatic intra-epithelial neoplasia. This phenotype is linked to increased expression of the histone methyl transferase EZH2 (Enhancer of Zeste Homolog 2), which results in the down-regulation of the tumor suppressors Msmb and Nkx3.1 through increased methylation of lysine 27 of histone H3 (H3K27) on their promoter regions. Altogether, our data provide a novel link between LXR, cholesterol homeostasis, and epigenetic control of tumor suppressor gene expression.
    PLoS Genetics 05/2013; 9(5):e1003483. DOI:10.1371/journal.pgen.1003483 · 8.17 Impact Factor
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    ABSTRACT: Lipids play a complex role in prostate cancer (PCa). Increased de novo synthesis of fatty acids and/or cholesterol is associated with the development of prostate tumors. Liver X Receptors (LXRs) are members of the nuclear receptor family that regulates intracellular lipid homeostasis. Targeting the transcriptional activity of LXRs has, therefore, been proposed as a mechanism for attenuating the progression of PCa. Histone Deacetylases (HDACs), however, have a negative effect on LXR activity. Therefore, HDAC inhibition reduces intracellular cholesterol levels and thereby decreases tumor cell proliferation. LXRs and HDAC inhibitors can, therefore, inhibit tumor proliferation. This review discusses the interacting roles of lipids, LXRs and HDACs in the development of PCa, where increased lipid levels enhance HDAC activity thereby altering LXR-dependent regulation of cellular lipid homeostasis. It provides a new paradigm for the treatment of prostate cancer, where LXRs are activated and HDACs repressed.
    Biochemical pharmacology 04/2013; 86(1). DOI:10.1016/j.bcp.2013.04.005 · 4.65 Impact Factor
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    ABSTRACT: Recent studies underline the implication of Liver X Receptors (LXRs) in several prostate diseases such as benign prostatic hyperplasia (BPH) and prostate cancer. In order to understand the molecular mechanisms involved, we derived epithelial cells from dorsal prostate (MPECs) of wild type (WT) or Lxrαβ-/- mice. In the WT MPECs, our results show that LXR activation reduces proliferation and correlates with the modification of the AKT-survival pathway. Moreover, LXRs regulate lipid homeostasis with the regulation of Abca1, Abcg1 and Idol, and, in a lesser extent, Srebp1, Fas and Acc. Conversely cells derived from Lxrαβ-/- mice show a higher basal phosphorylation and consequently activation of the survival/proliferation transduction pathways AKT and MAPK. Altogether, our data point out that the cell model we developed allows deciphering the molecular mechanisms inducing the cell cycle arrest. Besides, we show that activated LXRs regulate AKT and MAPK transduction pathways and demonstrate that LXRs could be good pharmacological targets in prostate disease such as cancer.
    PLoS ONE 03/2013; 8(3):e58876. DOI:10.1371/journal.pone.0058876 · 3.53 Impact Factor
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    ABSTRACT: BACKGROUND & AIMS: Nutrients influence non alcoholic fatty liver disease. Essential fatty acids deficiency promotes various syndromes including hepatic steatosis through increased de novo lipogenesis. The mechanisms underlying such increased lipogenic response remain unidentified. METHODS: We used wild-type mice and mice lacking Liver X Receptors to perform a nutrigenomic study that aimed at examining the role of these transcription factors. RESULTS: We showed that, in the absence of Liver X Receptors, essential fatty acids deficiency does not promote steatosis. Consistent with this, Liver X Receptors are required for the elevated expression of genes involved in lipogenesis in response to essential fatty acids deficiency. CONCLUSION: This work identifies for the first time the central role of Liver X Receptors in steatosis induced by essential fatty acids deficiency.
    Journal of Hepatology 01/2013; 58(5). DOI:10.1016/j.jhep.2013.01.006 · 10.40 Impact Factor
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    ABSTRACT: Cholesterol is a fundamental molecule for life. Located in the cell membrane, this sterol participates to the cell signaling of growth factors. Inside the cell it can be converted in hormones such as androgens or modulate the immune response. Such important functions could not be solely dependent of external supply by diet hence de novo synthesis could occur from acetate in almost all mammalian cells. If a deficiency in cholesterol sourcing leads to development troubles, overstocking has been associated to various diseases such as atherosclerosis and can-cers. Cholesterol homeostasis should thus be tightly regulated at the uptake, de novo synthesis, storage and export processes. Various transcription factors have been described these last years as important to regulate cholesterol levels. Besides, synthetic molecules have been developed for many years to modulate cholesterol synthesis, such as statins. Many articles have associated prostate cancer, whose incidence is constantly increasing, to cholesterol disequilibrium. Targeting cholesterol could thus be a new pharmacological hit to counteract the initiation, develop-ment and/or progression of prostate cancer. Among the transcription factors regulating cholesterol homeostasis, the nuclear receptors Liver X Receptors (LXRs) control cholesterol uptake and export. Targeting the LXRs offers a new field of investigation to treat cancer. This review highlights the molecular relationships among LXRs, prostate cancer and cholesterol and why LXRs have good chance to be targeted one day in this tumor. LXRs, prostate cancer and cholesterol, more than a "Ménage à trois", The Good, the Bad and the Ugly.
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    ABSTRACT: Cholesterol is a fundamental molecule for life. Located in the cell membrane, this sterol participates to the cell signaling of growth factors. Inside the cell it can be converted in hormones such as androgens or modulate the immune response. Such important functions could not be solely dependent of external supply by diet hence de novo synthesis could occur from acetate in almost all mammalian cells. If a deficiency in cholesterol sourcing leads to development troubles, overstocking has been associated to various diseases such as atherosclerosis and cancers. Cholesterol homeostasis should thus be tightly regulated at the uptake, de novo synthesis, storage and export processes. Various transcription factors have been described these last years as important to regulate cholesterol levels. Besides, synthetic molecules have been developed for many years to modulate cholesterol synthesis, such as statins. Many articles have associated prostate cancer, whose incidence is constantly increasing, to cholesterol disequilibrium. Targeting cholesterol could thus be a new pharmacological hit to counteract the initiation, development and/or progression of prostate cancer. Among the transcription factors regulating cholesterol homeostasis, the nuclear receptors Liver X Receptors (LXRs) control cholesterol uptake and export. Targeting the LXRs offers a new field of investigation to treat cancer. This review highlights the molecular relationships among LXRs, prostate cancer and cholesterol and why LXRs have good chance to be targeted one day in this tumor. LXRs, prostate cancer and cholesterol, more than a "Ménage à trois", The Good, the Bad and the Ugly.
    American Journal of Cancer Research 01/2013; 3(1):58-69. · 3.97 Impact Factor
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    ABSTRACT: In the last decades, studies in rodents have highlighted links between in utero and/or neonatal exposures to molecules that alter endocrine functions and the development of genital tract abnormalities, such as cryptorchidism, hypospadias, and impaired spermatogenesis. Most of these molecules, called endocrine disrupters exert estrogenic and/or antiandrogenic activities. These data led to the hypothesis of the testicular dysgenesis syndrome which postulates that these disorders are one clinical entity and are linked by epidemiological and pathophysiological relations. Furthermore, infertility has been stated as a risk factor for testicular cancer (TC). The incidence of TC has been increasing over the past decade. Most of testicular germ cell cancers develop through a pre-invasive carcinoma in situ from fetal germ cells (primordial germ cell or gonocyte). During their development, fetal germ cells undergo epigenetic modifications. Interestingly, several lines of evidence have shown that gene regulation through epigenetic mechanisms (DNA and histone modifications) plays an important role in normal development as well as in various diseases, including TC. Here we will review chromatin modifications which can affect testicular physiology leading to the development of TC; and highlight potential molecular pathways involved in these alterations in the context of environmental exposures.
    Frontiers in Endocrinology 11/2012; 3:150. DOI:10.3389/fendo.2012.00150
  • Jean-Marc A Lobaccaro, Denis Gallot, Serge Lumbroso, Kevin Mouzat
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    ABSTRACT: The role of cholesterol in female reproductive physiology has been suspected for a long time, while the molecular bases were unknown. Cholesterol is the precursor of ovarian steroids biosynthesis and is also essential for fertility. In the uterus, cholesterol is essential to achieve correct contractions at term, but an excessive uterine cholesterol concentration has been associated with contractility defects. Liver X Receptor (LXR) alpha and LXR beta are nuclear receptors activated by oxysterols, oxidized derivatives of cholesterol. Since their discovery, the role of LXRs in the control of cholesterol homeostasis has been widely described. Beyond their cholesterol-lowering role, more recent data have linked these nuclear receptors to various physiological processes. In particular, they control ovarian endocrine and exocrine functions, as well as uterine contractility. Their contribution to female reproductive cancers will also be discussed. This review will try to enlighten on the LXRs as a molecular link between dietary cholesterol and reproductive diseases in women. In the future, a better comprehension of the various physiological processes regulated by the LXRs will help to develop new ligands to prevent or to cure these pathologies in women.
    Journal of endocrinological investigation 11/2012; 36(1). DOI:10.3275/8765 · 1.55 Impact Factor
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    ABSTRACT: The Liver X Receptors (LXRs) α and β and the peroxisome proliferator-activated receptor α (PPARα) are transcription factors that belong to class II nuclear receptors. They drive the expression of genes involved in hepatic lipid homeostasis and therefore are important targets for the prevention and treatment of nonalcoholic fatty liver disease (NAFLD). LXRs and PPARα are regulated by endogenous ligands, oxysterols and fatty acid derived molecules respectively. In the liver, pharmacological activation of LXRs leads to the over-expression of genes involved in de novo lipogenesis, while PPARα is critical for fatty acid catabolism in nutrient deprivation. Even if these two nuclear receptors seemed to play opposite parts, recent studies have highlighted that PPARα also influence the expression of genes involved in fatty acids synthesis. In this study, we used pharmacological approaches and genetically engineered mice to investigate the cross-talk between LXRs and PPARα in the regulation of genes responsible for lipogenesis. We first investigated the effect of T0901317 and fenofibrate, two synthetic agonists of LXRs and PPARα, respectively. As expected, T0901317 and fenofibrate induce expression of genes involved LXR-dependent and PPARα-dependent lipogenic responses. Considering such overlapping effect, we then tested whether LXR agonist may influence PPARα driven response and vice versa. We show that the lack of PPARα does not influence the effects of T0901317 on lipogenic genes expression. However, PPARα deficiency prevents the up-regulation of genes involved in ω-hydroxylation that are induced by the LXR agonist. In addition, over-expression of lipogenic genes in response to fenofibrate is decreased in LXR knockout mice as well as the expression of PPARα target genes involved in fatty acid oxidation. Altogether, our work provides in vivo evidence for a central interconnection between nuclear receptors that drive hepatic lipid metabolism in response to oxysterol and fatty acids.
    Biochimie 10/2012; 95(3). DOI:10.1016/j.biochi.2012.09.028 · 3.12 Impact Factor
  • Jean-Marc A Lobaccaro, Florence Brugnon, David H Volle, Silvère Baron
    Clinical Lipidology 10/2012; 7(5):485-488. DOI:10.2217/clp.12.58 · 0.86 Impact Factor

Publication Stats

4k Citations
329.52 Total Impact Points

Institutions

  • 2005–2015
    • Université Blaise Pascal - Clermont-Ferrand II
      • Laboratoire Génétique, Reproduction et Développement
      Clermont, Auvergne, France
  • 2008–2014
    • French National Centre for Scientific Research
      Lutetia Parisorum, Île-de-France, France
  • 2003–2013
    • French Institute of Health and Medical Research
      Lutetia Parisorum, Île-de-France, France
  • 2007–2012
    • Le Centre de Recherche en Nutrition Humaine Rhône-Alpes
      Pierre-Bénite, Rhône-Alpes, France
    • University of Auvergne
      Clermont, Auvergne, France
  • 1993–2008
    • Unité Inserm U1077
      Caen, Lower Normandy, France
  • 2000
    • University of Texas Southwestern Medical Center
      • Department of Pharmacology
      Dallas, TX, United States
  • 1998–2000
    • Howard Hughes Medical Institute
      Ashburn, Virginia, United States