SUCNR1-mediated chemotaxis of macrophages aggravates obesity-induced inflammation and diabetes

[1]  T. Junt,et al.  GPR91 senses extracellular succinate released from inflammatory macrophages and exacerbates rheumatoid arthritis , 2016, The Journal of experimental medicine.

[2]  Phillip G. Popovich,et al.  Novel Markers to Delineate Murine M1 and M2 Macrophages , 2015, PloS one.

[3]  P. Sepúlveda,et al.  Targeted Disruption of the SUCNR1 Metabolic Receptor Leads to Dichotomous Effects on Obesity , 2014, Diabetes.

[4]  C. Tack,et al.  Diabetes-Related Distress, Insulin Dose, and Age Contribute to Insulin-Associated Weight Gain in Patients With Type 2 Diabetes: Results of a Prospective Study , 2014, Diabetes Care.

[5]  H. Tilg,et al.  IL-37 protects against obesity-induced inflammation and insulin resistance , 2014, Nature Communications.

[6]  Jasmit Shah,et al.  Metabolic remodeling of white adipose tissue in obesity. , 2014, American journal of physiology. Endocrinology and metabolism.

[7]  C. Bing,et al.  Interleukin-1β mediates macrophage-induced impairment of insulin signaling in human primary adipocytes , 2014, American journal of physiology. Endocrinology and metabolism.

[8]  J. Sangiovanni,et al.  Deficiency in the metabolite receptor SUCNR1 (GPR91) leads to outer retinal lesions , 2013, Aging.

[9]  Liang Zheng,et al.  Succinate is an inflammatory signal that induces IL-1β through HIF-1α , 2013, Nature.

[10]  S. Gordon,et al.  Genetic programs expressed in resting and IL-4 alternatively activated mouse and human macrophages: similarities and differences. , 2013, Blood.

[11]  M. A. Saad,et al.  Modulation of gut microbiota by antibiotics improves insulin signalling in high-fat fed mice , 2012, Diabetologia.

[12]  J. Olefsky,et al.  The cellular and signaling networks linking the immune system and metabolism in disease , 2012, Nature Medicine.

[13]  P. Deen,et al.  The Succinate Receptor as a Novel Therapeutic Target for Oxidative and Metabolic Stress-Related Conditions , 2012, Front. Endocrin..

[14]  P. Scherer,et al.  Adipose tissue remodeling and obesity. , 2011, The Journal of clinical investigation.

[15]  J. Peti-Peterdi.  High glucose and renin release: the role of succinate and GPR91. , 2010, Kidney international.

[16]  P. Schauer,et al.  Adipocyte Apoptosis, a Link between Obesity, Insulin Resistance, and Hepatic Steatosis* , 2009, The Journal of Biological Chemistry.

[17]  T. Junt,et al.  Triggering the succinate receptor GPR91 on dendritic cells enhances immunity , 2008, Nature Immunology.

[18]  S. Coughlin,et al.  Anatomical Profiling of G Protein-Coupled Receptor Expression , 2008, Cell.

[19]  J. A. van der Laak,et al.  Peroxisome Proliferator-activated Receptor γ Activation Promotes Infiltration of Alternatively Activated Macrophages into Adipose Tissue* , 2008, Journal of Biological Chemistry.

[20]  M. Kaneki,et al.  Obesity-induced Insulin Resistance and Hyperglycemia: Etiologic Factors and Molecular Mechanisms , 2008, Anesthesiology.

[21]  Elliott J. Meer,et al.  Succinate receptor GPR91 provides a direct link between high glucose levels and renin release in murine and rabbit kidney. , 2008, The Journal of clinical investigation.

[22]  T. Major,et al.  Circulating succinate is elevated in rodent models of hypertension and metabolic disease. , 2007, American journal of hypertension.

[23]  W. Ouwehand,et al.  Comparative gene expression profiling of in vitro differentiated megakaryocytes and erythroblasts identifies novel activatory and inhibitory platelet membrane proteins. , 2007, Blood.

[24]  A. Saltiel,et al.  Obesity induces a phenotypic switch in adipose tissue macrophage polarization. , 2007, The Journal of clinical investigation.

[25]  Jinhai Gao,et al.  Citric acid cycle intermediates as ligands for orphan G-protein-coupled receptors , 2004, Nature.

[26]  J. Weinberg,et al.  Mitochondrial dysfunction during hypoxia/reoxygenation and its correction by anaerobic metabolism of citric acid cycle intermediates. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[27]  M. Papa,et al.  Tumor necrosis factor-alpha suppresses insulin-induced tyrosine phosphorylation of insulin receptor and its substrates. , 1993, The Journal of biological chemistry.

[28]  J. Ye.  Emerging role of adipose tissue hypoxia in obesity and insulin resistance , 2009, International Journal of Obesity.

[29]  M. Haneklaus,et al.  Succinate is an inflammatory signal that induces IL-1 beta through HIF-1 alpha , 2017 .