دورية أكاديمية
Circulating NOD1 Activators and Hematopoietic NOD1 Contribute to Metabolic Inflammation and Insulin Resistance.
| العنوان: | Circulating NOD1 Activators and Hematopoietic NOD1 Contribute to Metabolic Inflammation and Insulin Resistance. |
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| المؤلفون: | Chan KL; Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario M5G 0A4, Canada; Department of Physiology, University of Toronto, Toronto, Ontario M5S 1A8, Canada., Tam TH; Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario M5G 0A4, Canada., Boroumand P; Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario M5G 0A4, Canada; Department of Biochemistry, University of Toronto, Toronto, Ontario M5S 1A8, Canada., Prescott D; Department of Immunology, University of Toronto, Toronto, Ontario M5S 1A8, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario M5S 1A8, Canada., Costford SR; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario M5S 1A8, Canada., Escalante NK; Department of Immunology, University of Toronto, Toronto, Ontario M5S 1A8, Canada., Fine N; Matrix Dynamics Group, Faculty of Dentistry, University of Toronto, Toronto, Ontario M5S 3E2, Canada., Tu Y; Neurosciences and Mental Health Program, The Hospital for Sick Children, Toronto, Ontario M5G 0A4, Canada., Robertson SJ; Department of Immunology, University of Toronto, Toronto, Ontario M5S 1A8, Canada., Prabaharan D; Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario M5G 0A4, Canada., Liu Z; Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario M5G 0A4, Canada., Bilan PJ; Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario M5G 0A4, Canada., Salter MW; Department of Physiology, University of Toronto, Toronto, Ontario M5S 1A8, Canada; Neurosciences and Mental Health Program, The Hospital for Sick Children, Toronto, Ontario M5G 0A4, Canada., Glogauer M; Matrix Dynamics Group, Faculty of Dentistry, University of Toronto, Toronto, Ontario M5S 3E2, Canada., Girardin SE; Department of Immunology, University of Toronto, Toronto, Ontario M5S 1A8, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario M5S 1A8, Canada., Philpott DJ; Department of Immunology, University of Toronto, Toronto, Ontario M5S 1A8, Canada., Klip A; Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario M5G 0A4, Canada; Department of Physiology, University of Toronto, Toronto, Ontario M5S 1A8, Canada; Department of Biochemistry, University of Toronto, Toronto, Ontario M5S 1A8, Canada. Electronic address: amira@sickkids.ca. |
| المصدر: | Cell reports [Cell Rep] 2017 Mar 07; Vol. 18 (10), pp. 2415-2426. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Cell Press Country of Publication: United States NLM ID: 101573691 Publication Model: Print Cited Medium: Internet ISSN: 2211-1247 (Electronic) NLM ISO Abbreviation: Cell Rep Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: [Cambridge, MA] : Cell Press, c 2012- |
| مواضيع طبية MeSH: | Hematopoiesis*/drug effects , Insulin Resistance*, Inflammation/*metabolism , Inflammation/*pathology , Nod1 Signaling Adaptor Protein/*metabolism, Adipose Tissue/pathology ; Animals ; Cell Movement/drug effects ; Cell Polarity/drug effects ; Chemokine CXCL1/metabolism ; Chemotactic Factors/pharmacology ; Diet, High-Fat ; Disease Models, Animal ; Gene Deletion ; Glucose/metabolism ; Inflammation/complications ; Macrophages/drug effects ; Macrophages/metabolism ; Macrophages/pathology ; Mice ; Mice, Knockout ; Neutrophil Infiltration/drug effects ; Obesity/blood ; Obesity/complications ; Obesity/pathology |
| مستخلص: | Insulin resistance is a chronic inflammatory condition accompanying obesity or high fat diets that leads to type 2 diabetes. It is hypothesized that lipids and gut bacterial compounds in particular contribute to metabolic inflammation by activating the immune system; however, the receptors detecting these "instigators" of inflammation remain largely undefined. Here, we show that circulating activators of NOD1, a receptor for bacterial peptidoglycan, increase with high fat feeding in mice, suggesting that NOD1 could be a critical sensor leading to metabolic inflammation. Hematopoietic depletion of NOD1 did not prevent weight gain but protected chimeric mice against diet-induced glucose and insulin intolerance. Mechanistically, while macrophage infiltration of adipose tissue persisted, notably these cells were less pro-inflammatory, had lower CXCL1 production, and consequently, lower neutrophil chemoattraction into the tissue. These findings reveal macrophage NOD1 as a cell-specific target to combat diet-induced inflammation past the step of macrophage infiltration, leading to insulin resistance. (Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.) |
| معلومات مُعتمدة: | Canada CIHR |
| فهرسة مساهمة: | Keywords: NOD1; gut microbiome; inflammation; insulin resistance; macrophage; neutrophil; obesity |
| المشرفين على المادة: | 0 (Chemokine CXCL1) 0 (Chemotactic Factors) 0 (Nod1 Signaling Adaptor Protein) 0 (Nod1 protein, mouse) IY9XDZ35W2 (Glucose) |
| تواريخ الأحداث: | Date Created: 20170309 Date Completed: 20171128 Latest Revision: 20191210 |
| رمز التحديث: | 20240628 |
| DOI: | 10.1016/j.celrep.2017.02.027 |
| PMID: | 28273456 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 2211-1247 |
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| DOI: | 10.1016/j.celrep.2017.02.027 |