Hepatocyte Toll-like receptor 4 regulates obesity-induced inflammation and insulin resistance
Published 2014 View Full Article
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Title
Hepatocyte Toll-like receptor 4 regulates obesity-induced inflammation and insulin resistance
Authors
Keywords
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Journal
Nature Communications
Volume 5, Issue 1, Pages -
Publisher
Springer Nature
Online
2014-05-12
DOI
10.1038/ncomms4878
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Note: Only part of the references are listed.- The serine protease prostasin regulates hepatic insulin sensitivity by modulating TLR4 signalling
- (2014) Kohei Uchimura et al. Nature Communications
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- Dietary saturated fatty acids prime the NLRP3 inflammasome via TLR4 in dendritic cells-implications for diet-induced insulin resistance
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- Lipid-induced insulin resistance mediated by the proinflammatory receptor TLR4 requires saturated fatty acid–induced ceramide biosynthesis in mice
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- Macrophages, Inflammation, and Insulin Resistance
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- Interleukin-6 Signaling in Liver-Parenchymal Cells Suppresses Hepatic Inflammation and Improves Systemic Insulin Action
- (2010) F. Thomas Wunderlich et al. Cell Metabolism
- A Liver-Derived Secretory Protein, Selenoprotein P, Causes Insulin Resistance
- (2010) Hirofumi Misu et al. Cell Metabolism
- Systemic toll-like receptor ligands modify B-cell responses in human inflammatory bowel disease
- (2010) Marie McDonnell et al. INFLAMMATORY BOWEL DISEASES
- Hematopoietic Cell-Specific Deletion of Toll-like Receptor 4 Ameliorates Hepatic and Adipose Tissue Insulin Resistance in High-Fat-Fed Mice
- (2009) Maziyar Saberi et al. Cell Metabolism
- B cells from periodontal disease patients express surface Toll-like receptor 4
- (2009) H. Shin et al. JOURNAL OF LEUKOCYTE BIOLOGY
- Toll-like receptor 4 mediates synergism between alcohol and HCV in hepatic oncogenesis involving stem cell marker Nanog
- (2009) K. Machida et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Alternative M2 Activation of Kupffer Cells by PPARδ Ameliorates Obesity-Induced Insulin Resistance
- (2008) Justin I. Odegaard et al. Cell Metabolism
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