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1. Cannabinoid CB2 receptor potentiates obesity-associated inflammation, insulin resistance and hepatic steatosis.

Author

Vanessa Deveaux, Thomas Cadoudal, Yasukatsu Ichigotani, Fatima Teixeira-Clerc, Alexandre Louvet, Sylvie Manin, Jeanne Tran-Van Nhieu, Marie Pierre Belot, Andreas Zimmer, Patrick Even, Patrice D Cani, Claude Knauf, Remy Burcelin, Adeline Bertola, Yannick Le Marchand-Brustel, Philippe Gual, Ariane Mallat, and Sophie Lotersztajn

Subjects
Medicine, Science
Abstract

BACKGROUND: Obesity-associated inflammation is of critical importance in the development of insulin resistance and non-alcoholic fatty liver disease. Since the cannabinoid receptor CB2 regulates innate immunity, the aim of the present study was to investigate its role in obesity-induced inflammation, insulin resistance and fatty liver. METHODOLOGY: Murine obesity models included genetically leptin-deficient ob/ob mice and wild type (WT) mice fed a high fat diet (HFD), that were compared to their lean counterparts. Animals were treated with pharmacological modulators of CB2 receptors. Experiments were also performed in mice knock-out for CB2 receptors (Cnr2 -/-). PRINCIPAL FINDINGS: In both HFD-fed WT mice and ob/ob mice, Cnr2 expression underwent a marked induction in the stromal vascular fraction of epididymal adipose tissue that correlated with increased fat inflammation. Treatment with the CB2 agonist JWH-133 potentiated adipose tissue inflammation in HFD-fed WT mice. Moreover, cultured fat pads isolated from ob/ob mice displayed increased Tnf and Ccl2 expression upon exposure to JWH-133. In keeping, genetic or pharmacological inactivation of CB2 receptors decreased adipose tissue macrophage infiltration associated with obesity, and reduced inductions of Tnf and Ccl2 expressions. In the liver of obese mice, Cnr2 mRNA was only weakly induced, and CB2 receptors moderately contributed to liver inflammation. HFD-induced insulin resistance increased in response to JWH-133 and reduced in Cnr2 -/- mice. Finally, HFD-induced hepatic steatosis was enhanced in WT mice treated with JWH-133 and blunted in Cnr2 -/- mice. CONCLUSION/SIGNIFICANCE: These data unravel a previously unrecognized contribution of CB2 receptors to obesity-associated inflammation, insulin resistance and non-alcoholic fatty liver disease, and suggest that CB2 receptor antagonists may open a new therapeutic approach for the management of obesity-associated metabolic disorders.

Published
2009
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2. Cannabinoid CB2 receptor potentiates obesity-associated inflammation, insulin resistance and hepatic steatosis

Author

Yannick Le Marchand-Brustel, Fatima Teixeira-Clerc, Sophie Lotersztajn, Thomas Cadoudal, Patrice D. Cani, Claude Knauf, Adeline Bertola, Alexandre Louvet, Marie Pierre Belot, Rémy Burcelin, Philippe Gual, Sylvie Manin, Jeanne Tran Van Nhieu, Ariane Mallat, Patrick C. Even, Vanessa Deveaux, Yasukatsu Ichigotani, Andreas Zimmer, Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-IFR10, Faculté de médecine, Université Paris-Est Marne-la-Vallée (UPEM), Département de pathologie [Mondor], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Department of Molecular Psychiatry, Rheinische Friedrich-Wilhelms-Universität Bonn, Physiologie de la Nutrition et du Comportement Alimentaire (PNCA), Institut National de la Recherche Agronomique (INRA)-AgroParisTech, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre méditérannéen de médecine moléculaire (C3M), Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Digestive Center, Centre Hospitalier Universitaire de Nice (CHU Nice), Service d'hépato-gastro-entérologie [APHP Henri Mondor], Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Nice Sophia Antipolis (1965 - 2019) (UNS), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), AgroParisTech-Institut National de la Recherche Agronomique (INRA), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM), UCL - MD/FARM - Ecole de pharmacie, and Simon, Marie Francoise

Subjects
Leptin, Male, Adipose tissue, lcsh:Medicine, Leptin - metabolism, Diabetes and Endocrinology/Obesity, Mice, 0302 clinical medicine, Adipocytes, Cannabinoid receptor type 2, lcsh:Science, Mice, Knockout, 0303 health sciences, Multidisciplinary, Chemistry, Fatty liver, Stromal vascular fraction, 3. Good health, Diabetes and Endocrinology, Triglycerides - metabolism, Adipose Tissue, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], lipids (amino acids, peptides, and proteins), medicine.symptom, Research Article, medicine.medical_specialty, Mice, Transgenic, Inflammation, Gastroenterology and Hepatology, 03 medical and health sciences, Insulin resistance, Internal medicine, medicine, Animals, [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Obesity, Triglycerides, 030304 developmental biology, Adipocytes - metabolism, Adipose Tissue - metabolism, lcsh:R, Neurosciences, medicine.disease, Fatty Liver, Mice, Inbred C57BL, Endocrinology, Neurons and Cognition, lcsh:Q, Insulin Resistance, Steatosis, Fatty Liver - complications, therapy, 030217 neurology & neurosurgery, Obesity - complications, therapy
Abstract

International audience; BACKGROUND: Obesity-associated inflammation is of critical importance in the development of insulin resistance and non-alcoholic fatty liver disease. Since the cannabinoid receptor CB2 regulates innate immunity, the aim of the present study was to investigate its role in obesity-induced inflammation, insulin resistance and fatty liver. METHODOLOGY: Murine obesity models included genetically leptin-deficient ob/ob mice and wild type (WT) mice fed a high fat diet (HFD), that were compared to their lean counterparts. Animals were treated with pharmacological modulators of CB2 receptors. Experiments were also performed in mice knock-out for CB2 receptors (Cnr2 -/-). PRINCIPAL FINDINGS: In both HFD-fed WT mice and ob/ob mice, Cnr2 expression underwent a marked induction in the stromal vascular fraction of epididymal adipose tissue that correlated with increased fat inflammation. Treatment with the CB2 agonist JWH-133 potentiated adipose tissue inflammation in HFD-fed WT mice. Moreover, cultured fat pads isolated from ob/ob mice displayed increased Tnf and Ccl2 expression upon exposure to JWH-133. In keeping, genetic or pharmacological inactivation of CB2 receptors decreased adipose tissue macrophage infiltration associated with obesity, and reduced inductions of Tnf and Ccl2 expressions. In the liver of obese mice, Cnr2 mRNA was only weakly induced, and CB2 receptors moderately contributed to liver inflammation. HFD-induced insulin resistance increased in response to JWH-133 and reduced in Cnr2 -/- mice. Finally, HFD-induced hepatic steatosis was enhanced in WT mice treated with JWH-133 and blunted in Cnr2 -/- mice. CONCLUSION/SIGNIFICANCE: These data unravel a previously unrecognized contribution of CB2 receptors to obesity-associated inflammation, insulin resistance and non-alcoholic fatty liver disease, and suggest that CB2 receptor antagonists may open a new therapeutic approach for the management of obesity-associated metabolic disorders.

Published
2009
Full Text
View/download PDF

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