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1. Psychobiotics for Patients with Chronic Gastrointestinal Disorders Having Anxiety or Depression Symptoms

Author

Thi Thu Trang Tran, Long Bao Hoang, Viet Hang Dao, Thi Oanh Trinh, and Van Long Dao

Subjects
medicine.medical_specialty, Constitutional symptoms, Hospital Anxiety and Depression Scale, 03 medical and health sciences, 0302 clinical medicine, Quality of life, Internal medicine, medicine, 030212 general & internal medicine, Case report form, General Nursing, Irritable bowel syndrome, Depression (differential diagnoses), Original Research, business.industry, Journal of Multidisciplinary Healthcare, 030503 health policy & services, General Medicine, anxiety, medicine.disease, Diarrhea, probiotics, depression, Anxiety, medicine.symptom, 0305 other medical science, business
Abstract

Viet Hang Dao,1,2 Long Bao Hoang,2 Thi Oanh Trinh,2 Thi Thu Trang Tran,2 Van Long Dao1,2 1Internal Medicine Faculty, Hanoi Medical University, Hanoi, Vietnam; 2Research and Training Management Unit, Institute of Gastroenterology and Hepatology, Hanoi, VietnamCorrespondence: Viet Hang Dao Email daoviethang@hmu.edu.vnPurpose: Using psychobiotics to modify the gut microbiome has been shown to improve the anxiety and depression situation of patients with chronic gastrointestinal (GI) symptoms. This study evaluated changes in depression, anxiety, GI symptomss and side effects when patients used a multispecies probiotics product.Patients and Methods: A single-center uncontrolled trial was conducted in patients with chronic GI symptoms, anxiety and depression who used a multispecies probiotics product. The patients were screened for anxiety and depression symptoms using the Hospital Anxiety and Depression Scale (HADS). Those who had a component score of 8 or higher were given the multispecies probiotics product for 2 months and followed up after 1 and 2 months. All data are collected and managed in a case report form.Results: Eighty-three patients were enrolled, with a mean age (SD) of 43.9 (12.3) years; 73.5% of the patients were female. Of these patients, 8 met the Rome IV criteria for irritable bowel syndrome. The HADS scores displayed significant improvement at follow-up. The mean (SD) total HADS scores were 20.0 (6.3), 7.2 (5.4), and 4.9 (5.1) at baseline, 1 month, and 2 months, respectively. Quality of life also improved significantly. A small proportion (< 5%) of patients developed mild symptoms, including fullness, diarrhea, and sleep complaints.Conclusion: After 2 months using the probiotic product, the symptoms of anxiety and depression improved significantly. Mild gastrointestinal or constitutional symptoms developed in some patients.Keywords: probiotics, anxiety, depression

Published
2021
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2. Lipoprotein(a) Cellular Uptake Ex Vivo and Hepatic Capture In Vivo Is Insensitive to PCSK9 Inhibition With Alirocumab

Author

Jean-Christophe Le Bail, BS Valentin Blanchard, Sophie Ho-Van-Guimbal, Sandra Beeské, Gihad Dargazanli, Thi Thu Trang Tran, Marie-Pierre Pruniaux, Mikaël Croyal, Olivier Bergis, Etienne Guillot, Denis Boulay, Gilles Lambert, BS Kévin Chemello, Philip Janiak, Elise F. Villard, Bruno Poirier, Lallemant, Pascal, CHOPIN - - CHOPIN2016 - ANR-16-RHUS-0007 - RHUS - VALID, Diabète athérothrombose et thérapies Réunion Océan Indien (DéTROI), Université de La Réunion (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Physiopathologie des Adaptations Nutritionnelles (PhAN), Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Sanofi Aventis R&D [Chilly-Mazarin], ANR-16-RHUS-0007,CHOPIN,CHOPIN(2016), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de La Réunion (UR)

Subjects
0301 basic medicine, biology, Chemistry, PCSK9, liver-humanized mice, [SDV]Life Sciences [q-bio], Endogeny, Lipoprotein(a), 030204 cardiovascular system & hematology, Pharmacology, 3. Good health, [SDV] Life Sciences [q-bio], 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, low-density lipoprotein receptor, proprotein convertase subtilisin/kexin type 9, In vivo, lipoprotein(a), LDL receptor, biology.protein, Cardiology and Cardiovascular Medicine, Ex vivo, Alirocumab, Lipoprotein
Abstract

International audience; Lipoprotein(a) (Lp[a]) is the most common genetically inherited risk factor for cardiovascular disease. Many aspects of Lp(a) metabolism remain unknown. We assessed the uptake of fluorescent Lp(a) in primary human lymphocytes as well as Lp(a) hepatic capture in a mouse model in which endogenous hepatocytes have been ablated and replaced with human ones. Modulation of LDLR expression with the PCSK9 inhibitor alirocumab did not alter the cellular or the hepatic uptake of Lp(a), demonstrating that the LDL receptor is not a major route for Lp(a) plasma clearance. These results have clinical implications because they underpin why statins are not efficient at reducing Lp(a). (C) 2020 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation.

Published
2020
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3. PCSK9 inhibition with alirocumab reduces lipoprotein(a) levels in nonhuman primates by lowering apolipoprotein(a) production rate

Author

Ilya Khantalin, Stéphane Ramin-Mangata, Brice Nativel, Stéphanie Billon-Crossouard, Mikaël Croyal, Rose Hélène Blanchard, Etienne Guillot, Kévin Chemello, Michel Krempf, Valentin Blanchard, Gilles Lambert, Audrey Aguesse, Bruno Poirier, Philip Janiak, Elise F. Villard, Christophe Boixel, Jean-Christophe Le Bail, Aurélie Thedrez, Thi-Thu-Trang Tran, Nutrition périnatale [Nantes] (Centres de Recherche en Nutrition Humaine - CRNH), Centre de Recherche en Nutrition Humaine - Ouest, Sanofi-Aventis R&D, SANOFI Recherche, Physiologie des Adaptations Nutritionnelles [UMR_A1280] (PhAN), Institut National de la Recherche Agronomique (INRA)-Université de Nantes (UN), Diabète athérothrombose et thérapies Réunion Océan Indien (DéTROI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de La Réunion (UR), Groupe d'Etude sur l'Inflammation Chronique et l'Obésité (GEICO), Université de La Réunion (UR), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), INRA: UMR1280 Physiologie des adaptations (UMR1280), Institut National de la Recherche Agronomique (INRA), Bureau d'Économie Théorique et Appliquée (BETA), Institut National de la Recherche Agronomique (INRA)-Université de Strasbourg (UNISTRA)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS), Physiopathologie des Adaptations Nutritionnelles (PhAN), and Université de Nantes (UN)-Institut National de la Recherche Agronomique (INRA)

Subjects
Male, 0301 basic medicine, medicine.medical_specialty, plasma lipoproteins, Apolipoprotein B, [SDV]Life Sciences [q-bio], receptors, 030204 cardiovascular system & hematology, Antibodies, Monoclonal, Humanized, Apoprotein(a), PCSK9, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, low-density lipoproteins, medicine, Animals, Receptor, ComputingMilieux_MISCELLANEOUS, Alirocumab, Cross-Over Studies, biology, Chemistry, Catabolism, Anticholesteremic Agents, PCSK9 Inhibitors, Antibodies, Monoclonal, General Medicine, Lipoprotein(a), Lipids, Macaca fascicularis, Cholesterol, 030104 developmental biology, Endocrinology, biology.protein, Kexin, Female, lipids (amino acids, peptides, and proteins), Lipoprotein
Abstract

Therapeutic antibodies targeting proprotein convertase subtilisin kexin type 9 (PCSK9) (e.g. alirocumab) lower low-density lipoprotein cholesterol (LDL-C) and lipoprotein (a) [Lp(a)] levels in clinical trials. We recently showed that PCSK9 enhances apolipoprotein(a) [apo(a)] secretion from primary human hepatocytes but does not affect Lp(a) cellular uptake. Here, we aimed to determine how PCSK9 neutralization modulates Lp(a) levels in vivo. Six nonhuman primates (NHP) were treated with alirocumab or a control antibody (IgG1) in a crossover protocol. After the lowering of lipids reached steady state, NHP received an intravenous injection of [2H3]-leucine, and blood samples were collected sequentially over 48 h. Enrichment of apolipoproteins in [2H3]-leucine was assessed by liquid chromatography–tandem mass spectrometry (LC–MS/MS). Kinetic parameters were calculated using numerical models with the SAAMII software. Compared with IgG1, alirocumab significantly reduced total cholesterol (TC) (−28%), LDL-C (−67%), Lp(a) (−56%), apolipoprotein B100 (apoB100) (−53%), and apo(a) (−53%). Alirocumab significantly increased the fractional catabolic rate of apoB100 (+29%) but not that of apo(a). Conversely, alirocumab sharply and significantly reduced the production rate (PR) of apo(a) (−42%), but not significantly that of apoB100, compared with IgG1, respectively. In line with the observations made in human hepatocytes, the present kinetic study establishes that PCSK9 neutralization with alirocumab efficiently reduces circulating apoB100 and apo(a) levels by distinct mechanisms: apoB primarily by enhancing its catabolism and apo(a) primarily by lowering its production.

Published
2018
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4. Short Term Palmitate Supply Impairs Intestinal Insulin Signaling via Ceramide Production

Author

Armelle Leturque, Agnieszka Blachnio-Zabielska, Véronique Carrière, Sylvie Demignot, Eric Hajduch, Jean-Paul Pais de Barros, Pascal Ferré, Bárbara Graziela Postal, Agnès Ribeiro, Céline Osinski, Monique Rousset, Thi Thu Trang Tran, Centre de Recherche des Cordeliers ( CRC ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Université Pierre et Marie Curie - Paris 6 ( UPMC ) -École pratique des hautes études ( EPHE ) -Université Paris Diderot - Paris 7 ( UPD7 ), Lipides - Nutrition - Cancer (U866) ( LNC ), Université de Bourgogne ( UB ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon ( ENSBANA ), Medical University of Bialystok, Physiologie de la Nutrition et Toxicologie (NUTox) (U866, Lipides et nutrition, équipe 7) (NUTox), Lipides - Nutrition - Cancer (U866) (LNC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bourgogne (UB)-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bourgogne (UB)-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, Centre de Recherche des Cordeliers (CRC), Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de santé publique et informatique médicale INSERM U872, Université Pierre et Marie Curie - Paris 6 (UPMC), Unité de génétique somatique, Institut Curie [Paris], Plateforme Lipidomique [Dijon] (LAP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bourgogne (UB)-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bourgogne (UB)-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-IFR100 - Structure fédérative de recherche Santé-STIC-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Bialystok Med Univ, Centre de Recherche des Cordeliers (CRC (UMR_S 872)), Université Paris Descartes - Paris 5 (UPD5)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Pathologies nutritionnelles et métaboliques : obésité et diabète, Université Pierre et Marie Curie - Paris 6 (UPMC)-IFR58-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA), Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Curie, Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-IFR100 - Structure fédérative de recherche Santé-STIC-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Paris Diderot - Paris 7 ( UPD7 ) -École pratique des hautes études ( EPHE ) -Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Université Pierre et Marie Curie - Paris 6 (UPMC)-École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA), Medical University of Białystok (MUB), Université Pierre et Marie Curie - Paris 6 (UPMC)-École pratique des hautes études (EPHE), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bourgogne (UB)-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement

Subjects
0301 basic medicine, medicine.medical_specialty, Ceramide, medicine.medical_treatment, Palmitic Acid, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Palm Oil, Ceramides, Biochemistry, Palmitic acid, Mice, 03 medical and health sciences, chemistry.chemical_compound, Insulin resistance, [ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathology, Internal medicine, medicine, Animals, Humans, Insulin, Plant Oils, Intestinal Mucosa, Phosphorylation, Molecular Biology, ComputingMilieux_MISCELLANEOUS, 2. Zero hunger, biology, Triglyceride, Cell Biology, Lipid signaling, medicine.disease, Lipids, 3. Good health, Insulin receptor, Enterocytes, 030104 developmental biology, Endocrinology, chemistry, Saturated fatty acid, biology.protein, Caco-2 Cells, Proto-Oncogene Proteins c-akt, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Signal Transduction
Abstract

International audience; The worldwide prevalence of metabolic diseases is increasing, and there are global recommendations to limit consumption of certain nutrients, especially saturated lipids. Insulin resistance, a common trait occurring in obesity and type 2 diabetes, is associated with intestinal lipoprotein overproduction. However, the mechanisms by which the intestine develops insulin resistance in response to lipid overload remain unknown. Here, we show that insulin inhibits triglyceride secretion and intestinal microsomal triglyceride transfer protein expression in vivo in healthy mice force-fed monounsaturated fatty acid-rich olive oil but not in mice force-fed saturated fatty acid-rich palm oil. Moreover, when mouse intestine and human Caco-2/TC7 enterocytes were treated with the saturated fatty acid, palmitic acid, the insulin-signaling pathway was impaired. We show that palmitic acid or palm oil increases ceramide production in intestinal cells and that treatment with a ceramide analogue partially reproduces the effects of palmitic acid on insulin signaling. In Caco-2/TC7 enterocytes, ceramide effects on insulin-dependent AKT phosphorylation are mediated by protein kinase C but not by protein phosphatase 2A. Finally, inhibiting de novo ceramide synthesis improves the response of palmitic acid-treated Caco-2/TC7 enterocytes to insulin. These results demonstrate that a palmitic acid-ceramide pathway accounts for impaired intestinal insulin sensitivity, which occurs within several hours following initial lipid exposure.

Published
2016
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5. Deregulated Lipid Sensing by Intestinal CD36 in Diet-Induced Hyperinsulinemic Obese Mouse Model

Author

Thi Thu Trang Tran, Nada A. Abumrad, Sinju Sundaresan, Hélène Poirier, Kévin Gaire, Véronique Traynard, Philippe Besnard, Isabelle Niot, Marjorie Buttet, Physiologie de la Nutrition et Toxicologie (NUTox) (U866, Lipides et nutrition, équipe 7) (NUTox), Lipides - Nutrition - Cancer (U866) (LNC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bourgogne (UB)-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bourgogne (UB)-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bourgogne (UB)-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, University of Michigan [Ann Arbor], University of Michigan System, Department of Cell Biology and Physiology Washington University School of Medicine 660 South Euclid Avenue St. Louis, Washington University in Saint Louis (WUSTL), Physiologie de la Nutrition et Toxicologie (NUTox) (U866, Lipides et nutrition, équipe 7) ( NUTox ), Lipides - Nutrition - Cancer (U866) ( LNC ), Université de Bourgogne ( UB ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon ( ENSBANA ) -Université de Bourgogne ( UB ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon ( ENSBANA ), Université de Bourgogne ( UB ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon ( ENSBANA ), and University of Michigan School of Medicine

Subjects
0301 basic medicine, CD36 Antigens, [SDV]Life Sciences [q-bio], lcsh:Medicine, 030204 cardiovascular system & hematology, Lipoprotein Metabolism, Mice, 0302 clinical medicine, Intestinal mucosa, Hyperinsulinemia, Intestinal Mucosa, lcsh:Science, Metabolic Syndrome, education.field_of_study, Multidisciplinary, Intestinal lipid absorption, 3. Good health, Postprandial, Chain Fatty-Acids, lipids (amino acids, peptides, and proteins), Research Article, Nonfasting Triglycerides, medicine.medical_specialty, Population, Transport, Distal Intestine, Biology, Diet, High-Fat, Absorption, 03 medical and health sciences, Insulin resistance, Internal medicine, Hyperinsulinism, medicine, Animals, Cholesterol Uptake, Obesity, education, Secretion, [ SDV ] Life Sciences [q-bio], Insulin-Resistance, lcsh:R, Hypertriglyceridemia, Lipid metabolism, medicine.disease, Lipid Metabolism, Disease Models, Animal, 030104 developmental biology, Endocrinology, Gene Expression Regulation, lcsh:Q, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
Abstract

International audience; The metabolic syndrome (MetS) greatly increases risk of cardiovascular disease and diabetes and is generally associated with abnormally elevated postprandial triglyceride levels. We evaluated intestinal synthesis of triglyceride-rich lipoproteins (TRL) in a mouse model of the MetS obtained by feeding a palm oil-rich high fat diet (HFD). By contrast to control mice, MetS mice secreted two populations of TRL. If the smaller size population represented 44% of total particles in the beginning of intestinal lipid absorption in MetS mice, it accounted for only 17% after 4 h due to the secretion of larger size TRL. The MetS mice displayed accentuated postprandial hypertriglyceridemia up to 3 h due to a defective TRL clearance. These alterations reflected a delay in lipid induction of genes for key proteins of TRL formation (MTP, L-FABP) and blood clearance (ApoC2). These abnormalities associated with blunted lipid sensing by CD36, which is normally required to optimize jejunal formation of large TRL. In MetS mice CD36 was not downregulated by lipid in contrast to control mice. Treatment of controls with the proteosomal inhibitor MG132, which prevented CD36 downregulation, resulted in blunted lipid-induction of MTP, L-FABP and ApoC2 gene expression, as in MetS mice. Absence of CD36 sensing was due to the hyperinsulinemia in MetS mice. Acute insulin treatment of controls before lipid administration abolished CD36 downregulation, lipid-induction of TRL genes and reduced postprandial triglycerides (TG), while streptozotocin-treatment of MetS mice restored lipid-induced CD36 degradation and TG secretion. In vitro, insulin treatment abolished CD36-mediated up-regulation of MTP in Caco-2 cells. In conclusion, HFD treatment impairs TRL formation in early stage of lipid absorption via insulin-mediated inhibition of CD36 lipid sensing. This impairment results in production of smaller TRL that are cleared slowly from the circulation, which might contribute to the reported association of CD36 variants with MetS risk.

Published
2016
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6. Mécanisme d’absorption intestinale des acides gras à longue chaîne : rôle émergent du CD36

Author

Hélène Poirier, Isabelle Niot, Marjorie Buttet, Thi Thu Trang Tran, Philippe Besnard, Véronique Traynard, Physiologie de la Nutrition et Toxicologie (NUTox) (U866, Lipides et nutrition, équipe 7) (NUTox), Lipides - Nutrition - Cancer (U866) (LNC), and Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)

Subjects
lipid absorption, [SDV]Life Sciences [q-bio], CD36, Postprandial hypertriglyceridemia, Medicine (miscellaneous), lcsh:TP670-699, intestinal adaptation, Hypertriglycéridémie postprandiale, 030204 cardiovascular system & hematology, Biochemistry, Intestinal absorption, 03 medical and health sciences, 0302 clinical medicine, Lipid-binding proteins, Chylomicrons, medicine, Cd36, intestine, sensing, 030304 developmental biology, Intestinal lipid absorption, 0303 health sciences, Nutrition and Dietetics, biology, Chemistry, Hypertriglyceridemia, medicine.disease, Molecular biology, Small intestine, 3. Good health, Bioavailability, medicine.anatomical_structure, Postprandial, biology.protein, lipids (amino acids, peptides, and proteins), lcsh:Oils, fats, and waxes, Absorption intestinale des lipides, Long chain fatty acid, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition, Food Science, Chylomicron
Abstract

International audience; Excessive lipid intake, associated with a qualitative imbalance, favors the development of obesity and associated diseases. Among the organs involved in lipid homeostasis, the small intestine remains the most poorly known although it is responsible for the lipid bioavailability and largely contributes to the regulation of postprandial hypertriglyceridemia. The mechanism of long chain fatty acid (LCFA) intestinal absorption is not totally elucidated. The synthesis of recent literature indicates that the intestine is able to adapt its absorption capacity to the fat content of the diet. This adaptation takes place through a fat-coordinated induction of LBP and apolipoproteins. CD36 could operate as a lipid sensor responsible for a transducing signal related to the lipid content of the diet at the origin of this intestinal adaptation. This lipid-mediated metabolic response may lead to the formation of large chylomicrons rapidly degraded in the blood. All together, these new data indicate that this intestinal lipid sensing mechanism may be a therapeutic target for reducing the postprandial hypertriglyceridemia and associated cardiovascular risks.; L’apport excessif de lipides, associé à un déséquilibre qualitatif, favorise le développement de l’obésité et des maladies associées. Parmi les organes impliqués dans l’homéostasie lipidique, l’intestin est le moins étudié alors qu’il contribue à la biodisponibilité des lipides et à l’hypertriglycéridémie postprandiale. Le mécanisme d’absorption des lipides n’est pas totalement élucidé mais, contrairement à ce qui est établi, l’intestin adapte ses capacités d’absorption en fonction de la quantité de lipides du régime. Cette adaptation s’exerce via la modulation des gènes impliqués dans la formation des chylomicrons, comme les lipid-binding proteins (LBP) et certaines apolipoprotéines. Une LBP membranaire, le CD36 serait un senseur des lipides entérocytaires qui, via la transduction d’un signal intracellulaire, déclencherait l’induction du niveau des protéines optimisant la sécrétion de chylomicrons plus rapidement dégradés au niveau sanguin. Le CD36 constituerait une nouvelle cible permettant de réduire l’hypertriglycéridémie postprandiale, facteur de risque des maladies cardiovasculaires.

Published
2012
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7. Luminal Lipid Regulates CD36 Levels and Downstream Signaling to Stimulate Chylomicron Synthesis

Author

Maurice M.A.L. Pelsers, Marie Claude Monnot, Jan F. C. Glatz, Pascal Degrace, Fatiha Nassir, Valérie Petit, Philippe Besnard, Lionel C. Clement, Nada A. Abumrad, Hélène Poirier, Isabelle Niot, Thi Thu Trang Tran, Physiologie de la Nutrition et Toxicologie (NUTox) (U866, Lipides et nutrition, équipe 7) (NUTox), Lipides - Nutrition - Cancer (U866) (LNC), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA), Department of Medicine, University of Washington, Department of Molecular Genetics [Maastricht, The Netherlands], Maastricht University [The Netherlands], Physiopathologie des Dyslipidémies (U866, Lipides et nutrition, équipe 6), Moleculaire Genetica, Genetica & Celbiologie, and RS: CARIM School for Cardiovascular Diseases

Subjects
CD36 Antigens, Male, MTP, CD36, [SDV]Life Sciences [q-bio], Biochemistry, Microsomal triglyceride transfer protein, Mice, 0302 clinical medicine, Intestinal mucosa, Cricetinae, Chylomicrons, Lipoprotein, Hypertriglyceridemia, Mice, Knockout, 0303 health sciences, Mitogen-Activated Protein Kinase 3, biology, Postprandial Period, Lipid-binding Protein, Intestine, ApoB48, ERK, medicine.anatomical_structure, Postprandial, lipids (amino acids, peptides, and proteins), Apolipoprotein B-48, MAP Kinase Signaling System, Enterocyte, CHO Cells, Chylomicron, 03 medical and health sciences, Cricetulus, parasitic diseases, medicine, Animals, Rats, Wistar, Molecular Biology, 030304 developmental biology, Ubiquitination, Lipid absorption, Lipid metabolism, Cell Biology, Lipid Metabolism, Rats, Enterocytes, Metabolism, biology.protein, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition, 030217 neurology & neurosurgery
Abstract

International audience; The membrane glycoprotein CD36 binds nanomolar concentrations of long chain fatty acids (LCFA) and is highly expressed on the luminal surface of enterocytes. CD36 deficiency reduces chylomicron production through unknown mechanisms. In this report, we provide novel insights into some of the underlying mechanisms. Our in vivo data demonstrate that CD36 gene deletion in mice does not affect LCFA uptake and subsequent esterification into triglycerides by the intestinal mucosa exposed to the micellar LCFA concentrations prevailing in the intestine. In rodents, the CD36 protein disappears early from the luminal side of intestinal villi during the postprandial period, but only when the diet contains lipids. This drop is significant 1 h after a lipid supply and associates with ubiquitination of CD36. Using CHO cells expressing CD36, it is shown that the digestion products LCFA and diglycerides trigger CD36 ubiquitination. In vivo treatment with the proteasome inhibitor MG132 prevents the lipid-mediated degradation of CD36. In vivo and ex vivo, CD36 is shown to be required for lipid activation of ERK1/2, which associates with an increase of the key chylomicron synthesis proteins, apolipoprotein B48 and microsomal triglyceride transfer protein. Therefore, intestinal CD36, possibly through ERK1/2-mediated signaling, is involved in the adaptation of enterocyte metabolism to the postprandial lipid challenge by promoting the production of large triglyceride-rich lipoproteins that are rapidly cleared in the blood. This suggests that CD36 may be a therapeutic target for reducing the postprandial hypertriglyceridemia and associated cardiovascular risks.

Published
2011
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8. Intestinal absorption of long-chain fatty acids: Evidence and uncertainties

Author

Thi Thu Trang Tran, Isabelle Niot, Philippe Besnard, Hélène Poirier, Physiologie de la Nutrition et Toxicologie (NUTox) (U866, Lipides et nutrition, équipe 7) (NUTox), Lipides - Nutrition - Cancer (U866) (LNC), and Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)

Subjects
[SDV]Life Sciences [q-bio], Biology, Fatty Acid-Binding Proteins, Biochemistry, Intestinal absorption, Chylomicron, 03 medical and health sciences, Mice, 0302 clinical medicine, Long-chain fatty acid, Lipid-binding protein, Chylomicrons, Intestine, Small, Animals, Humans, Gene, 030304 developmental biology, Cloning, Hypertriglyceridemia, 0303 health sciences, Cell Membrane, Fatty Acids, Cell Biology, Small intestine, Lipid Metabolism, Phenotype, Dietary Fats, Enterocytes, Intestinal Absorption, Health, lipids (amino acids, peptides, and proteins), Long chain fatty acid, Functional genomics, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition, 030217 neurology & neurosurgery, Lipoprotein
Abstract

International audience; Over the two last decades, cloning of proteins responsible for trafficking and metabolic fate of long-chain fatty acids (LCFA) in gut has provided new insights on cellular and molecular mechanisms involved in fat absorption. To this systematic cloning period, functional genomics has succeeded in providing a new set of surprises. Disruption of several genes, thought to play a crucial role in LCFA absorption, did not lead to clear phenotypes. This observation raises the question of the real physiological role of lipid-binding proteins and lipid-metabolizing enzymes expressed in enterocytes. The goal of this review is to analyze present knowledge concerning the main steps of intestinal fat absorption from LCFA uptake to lipoprotein release and to assess their impact on health.

Published
2009
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9. CD36 Displays Features of a Lipid-Sensor Involved in Chylomicron Processing in the Rodent Small Intestine

Author

Thi Thu Trang Tran, M.A.L. Pelsers, Marie-Claude Monnot, Isabelle Niot, Pascal Degrace, Hélène Poirier, Philippe Besnard, V. Petit, Fatiha Nassir, Jan F. C. Glatz, Lionel C. Clement, Nada A. Abumrad, Physiologie de la Nutrition et Toxicologie (NUTox) (U866, Lipides et nutrition, équipe 7) (NUTox), Lipides - Nutrition - Cancer (U866) (LNC), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA), Department of Medicine, University of Washington, Department of Molecular Genetics [Maastricht, The Netherlands], Maastricht University [The Netherlands], and Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)

Subjects
medicine.medical_specialty, Rodent, 030309 nutrition & dietetics, [SDV]Life Sciences [q-bio], CD36, 030209 endocrinology & metabolism, Gastroenterology, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, biology.animal, parasitic diseases, Internal Medicine, medicine, 0303 health sciences, biology, Chemistry, General Medicine, Small intestine, Cell biology, medicine.anatomical_structure, biology.protein, lipids (amino acids, peptides, and proteins), Cardiology and Cardiovascular Medicine, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition, Chylomicron
Abstract

International audience; The membrane glycoprotein CD36 binds nanomolar concentrations of long-chain fatty acids (LCFA) and is highly expressed on the luminal surface of enterocytes. CD36 deficiency reduces chylomicron production through unknown mechanisms.In this report, we provide novel insights into the potential underlying mechanisms. Our in vivo data demonstrated that CD36 gene deletion in mice did not affect LCFA uptake and their subsequent esterification into triglycerides by the intestinal mucosa at micellar LCFA concentrations prevailing in the intestine. In rodents, CD36 protein early disappeared from the luminal side of intestinal villi during the post-prandial period but only when the diet contained lipids. This drop was significant 1 h after a lipid supply and was associated with an ubiquitination of CD36 as reported during the ligand receptor desensitization process. Using CHO cells expressing CD36, it is shown that the digestion products, LCFA and diglycerides, triggered the CD36 ubiquitination. In vivo treatment with the proteasome inhibitor MG132 prevented the lipid-mediated degradation of CD36 and the up-regulation of L-FABP, a key gene implicated in the formation and secretion of large chylomicrons. Since the L-FABP up-regulation by lipids remained abolished in CD36-null mice with and without MG132, CD36 degradation appears to be linked to the chylomicron formation.Therefore, intestinal CD36 displays features of a lipid sensor involving in the adaptation of enterocyte metabolism to the post-prandial lipid challenge by producing large triglyceride-rich lipoproteins rapidly cleared in blood. This finding raises the possibility of alternative therapeutic approaches to reduce the post-prandial hypertriglyceridemia and prevent cardiovascular risks.

Published
2010
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