Resistin is expressed in human macrophages and directly regulated by PPARγ activators
By L. Patel, Amy C Buckels, I. Kinghorn, P. Murdock, J. Holbrook, C. Plumpton, C. Macphee, Stephen A. Smith. 2003
842 citations recorded by the source corpus.
Subfields: Epidemiology, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/ba10f9f7826920cdecdcfe9fe00ad0ad6e885c63
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Epidemiology
In Molecular Biology
- B. Spiegelman
- E. Rosen
- Mitchell A. Lazar
- Myung‐Sook Choi
- U. Jung
- M. Qatanani
- G. Steinberg
- R. Scarpulla
In Physiology
- B. Spiegelman
- E. Rosen
- Mitchell A. Lazar
- G. Steinberg
- M. Qatanani
- S. Galic
- J. Oakhill
- Myung‐Sook Choi
Citations in the corpus
- Adipocytes as regulators of energy balance and glucose homeostasis (2006, background): “The bulk of the data suggest that human resistin is the product of macrophages or other stromal cells within the fat pa”
- Obesity and Its Metabolic Complications: The Role of Adipokines and the Relationship between Obesity, Inflammation, Insulin Resistance, Dyslipidemia and Nonalcoholic Fatty Liver Disease (2014, background): “Unlike mouse resistin, human resistin is exclusively expressed in mononuclear cells including macrophages [126], and macrophage-derived human resistin exacerbates adipose tissue inflammation”
- Resistin, an Adipokine with Potent Proinflammatory Properties1 (2005, background): “Low levels of resistin are also expressed in lung tissue, resting endothelial cells, and in placenta (4).”
- Mechanisms of obesity-associated insulin resistance: many choices on the menu. (2007, background): “However, other studies failed to show such an association (Janke et al. 2002; Kielstein et al. 2003; Patel et al. 2003).”
- Adipose tissue as an endocrine organ. (2010, background): “Resistin is expressed within adipocytes of rodents (Steppan et al., 2001) and macrophages of humans (Patel et al., 2003) and its production is increased with feeding and obesity and decreased by PPAR ligands (Rajala et al., 2004).”