Targeted disruption of AdipoR1 and AdipoR2 causes abrogation of adiponectin binding and metabolic actions
暂无分享,去创建一个
P. Froguel | T. Kadowaki | A. Tsuchida | T. Yamauchi | Y. Hada | Yusuke Ito | T. Maki | Masaki Kobayashi | N. Kubota | I. Takamoto | T. Kubota | K. Ueki | K. Tobe | M. Iwabu | M. Awazawa | K. Tokuyama | R. Nagai | H. Kozono | J. Kamon | K. Hara | H. Ogata | T. Ide | M. Tsunoda | K. Kumagai | Y. Nio | T. Takazawa | M. Okada-Iwabu | Sachiko Kawamoto | K. Murakami | Toshiyuki Maki | Katsuyoshi Kumagai | Iseki Takamoto | Tetsuya Kubota | Miki Okada-Iwabu | Masato Iwabu | Tetsuya Kubota
[1] Y. Matsuzawa. The metabolic syndrome and adipocytokines , 2006, Expert review of clinical immunology.
[2] T. Kadowaki,et al. Overexpression of Monocyte Chemoattractant Protein-1 in Adipose Tissues Causes Macrophage Recruitment and Insulin Resistance* , 2006, Journal of Biological Chemistry.
[3] Kohjiro Ueki,et al. Adiponectin and adiponectin receptors in insulin resistance, diabetes, and the metabolic syndrome. , 2006, The Journal of clinical investigation.
[4] J. Zierath,et al. AMP-activated protein kinase signaling in metabolic regulation. , 2006, The Journal of clinical investigation.
[5] R. Kitazawa,et al. MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity. , 2006, The Journal of clinical investigation.
[6] T. Noda,et al. Pioglitazone Ameliorates Insulin Resistance and Diabetes by Both Adiponectin-dependent and -independent Pathways* , 2006, Journal of Biological Chemistry.
[7] N. Ruderman,et al. Mice Lacking Adiponectin Show Decreased Hepatic Insulin Sensitivity and Reduced Responsiveness to Peroxisome Proliferator-activated Receptor γ Agonists* , 2006, Journal of Biological Chemistry.
[8] Ichiro,et al. Overexpression of MCP-1 in adipose tissues causes macrophage recruitment and insulin resistance , 2006 .
[9] P. Scherer. From Lipid Storage Compartment to Endocrine Organ , 2006 .
[10] M. Magnuson,et al. The network of glucokinase-expressing cells in glucose homeostasis and the potential of glucokinase activators for diabetes therapy. , 2006, Diabetes.
[11] Takashi Kadowaki,et al. Combination , 2019, Understanding the Law of Assignment.
[12] K. Wellen,et al. Inflammation, stress, and diabetes. , 2005, The Journal of clinical investigation.
[13] H. Lodish,et al. The role of the adipocyte hormone adiponectin in cardiovascular disease. , 2005, Current opinion in pharmacology.
[14] Morihiro Matsuda,et al. Increased oxidative stress in obesity and its impact on metabolic syndrome. , 2004, The Journal of clinical investigation.
[15] Yuichi Harano,et al. PPARα ligands activate antioxidant enzymes and suppress hepatic fibrosis in rats , 2004 .
[16] P. Froguel,et al. Insulin/Foxo1 Pathway Regulates Expression Levels of Adiponectin Receptors and Adiponectin Sensitivity* , 2004, Journal of Biological Chemistry.
[17] H. Lodish,et al. T-cadherin is a receptor for hexameric and high-molecular-weight forms of Acrp30/adiponectin. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[18] T. Okanoue,et al. PPARalpha ligands activate antioxidant enzymes and suppress hepatic fibrosis in rats. , 2004, Biochemical and biophysical research communications.
[19] M. Desai,et al. Obesity is associated with macrophage accumulation in adipose tissue. , 2003, The Journal of clinical investigation.
[20] L. Tartaglia,et al. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. , 2003, The Journal of clinical investigation.
[21] Philippe Froguel,et al. Cloning of adiponectin receptors that mediate antidiabetic metabolic effects , 2003, Nature.
[22] P. Froguel,et al. Globular Adiponectin Protected ob/ob Mice from Diabetes and ApoE-deficient Mice from Atherosclerosis* , 2003, The Journal of Biological Chemistry.
[23] H. Lodish,et al. Enhanced muscle fat oxidation and glucose transport by ACRP30 globular domain: Acetyl–CoA carboxylase inhibition and AMP-activated protein kinase activation , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[24] M. Kasuga,et al. Hyperinsulinemia, glucose intolerance, and dyslipidemia induced by acute inhibition of phosphoinositide 3-kinase signaling in the liver. , 2002, The Journal of clinical investigation.
[25] S. Uchida,et al. Adiponectin stimulates glucose utilization and fatty-acid oxidation by activating AMP-activated protein kinase , 2002, Nature Medicine.
[26] Philippe Froguel,et al. Disruption of Adiponectin Causes Insulin Resistance and Neointimal Formation* , 2002, The Journal of Biological Chemistry.
[27] N. Socci,et al. Role for Stearoyl-CoA Desaturase-1 in Leptin-Mediated Weight Loss , 2002, Science.
[28] M. Matsuda,et al. Diet-induced insulin resistance in mice lacking adiponectin/ACRP30 , 2002, Nature Medicine.
[29] M. Brownlee. Biochemistry and molecular cell biology of diabetic complications , 2001, Nature.
[30] Y. Terauchi,et al. The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity , 2001, Nature Medicine.
[31] P. Scherer,et al. The adipocyte-secreted protein Acrp30 enhances hepatic insulin action , 2001, Nature Medicine.
[32] H. Lodish,et al. Proteolytic cleavage product of 30-kDa adipocyte complement-related protein increases fatty acid oxidation in muscle and causes weight loss in mice. , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[33] J. Lawrence,et al. Protection against oxidative stress-induced insulin resistance in rat L6 muscle cells by mircomolar concentrations of alpha-lipoic acid. , 2001, Diabetes.
[34] T. Awata,et al. The ligands/activators for peroxisome proliferator-activated receptor α (PPARα) and PPARγ increase Cu2+, Zn2+-superoxide dismutase and decrease p22phox message expressions in primary endothelial cells , 2001 .
[35] T. Awata,et al. The ligands/activators for peroxisome proliferator-activated receptor alpha (PPARalpha) and PPARgamma increase Cu2+,Zn2+-superoxide dismutase and decrease p22phox message expressions in primary endothelial cells. , 2001, Metabolism: clinical and experimental.
[36] D. Carling,et al. Characterization of the Role of AMP-Activated Protein Kinase in the Regulation of Glucose-Activated Gene Expression Using Constitutively Active and Dominant Negative Forms of the Kinase , 2000, Molecular and Cellular Biology.
[37] D. Hardie,et al. 5-aminoimidazole-4-carboxamide riboside mimics the effects of insulin on the expression of the 2 key gluconeogenic genes PEPCK and glucose-6-phosphatase. , 2000, Diabetes.
[38] Sander Kersten,et al. Roles of PPARs in health and disease , 2000, Nature.
[39] G. Shulman,et al. On Diabetes: Insulin Resistance Cellular Mechanisms of Insulin Resistance , 2022 .
[40] Frank J. Gonzalez,et al. Peroxisome Proliferator-activated Receptor α Negatively Regulates the Vascular Inflammatory Gene Response by Negative Cross-talk with Transcription Factors NF-κB and AP-1* , 1999, The Journal of Biological Chemistry.
[41] A. Rudich,et al. Prolonged oxidative stress impairs insulin-induced GLUT4 translocation in 3T3-L1 adipocytes. , 1998, Diabetes.
[42] W. Koenig,et al. Activation of human aortic smooth-muscle cells is inhibited by PPARα but not by PPARγ activators , 1998, Nature.
[43] B. Spiegelman,et al. Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance. , 1993, Science.