Inflammation and insulin resistance.
By Z. Bloomgarden. Diabetes Care, 2003
2,959 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology
View Paper: https://www.semanticscholar.org/paper/bba5332197f081282ba74b6ef7d36272f3eb6176
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Endocrinology, Diabetes and Metabolism
- A. Chawla
- Alan R. Saltiel
- M. Wymann
- H. Kwon
- J. Pessin
- R. Schneiter
- J. Odegaard
- Juan José Marín-Peñalver
In Epidemiology
- A. Chawla
- Jongsoon Lee
- Jerrold M. Olefsky
- Haiming Cao
- Alan R. Saltiel
- S. Shoelson
- C. Lumeng
- J. Odegaard
Citations in the corpus
- Fat Treg cells: a liaison between the immune and metabolic systems (2009, background): “There has been a parallel rise in the incidence of obesity, now recognized to be a major contributor to the insulin resistance underlying this spectrum of metabolic abnormalitie”
- Integration of metabolism and inflammation by lipid-activated nuclear receptors (2008, background): “Recently, it has become increasingly clear that inflammation that is mediated by tissue-resident macrophages is an essential component of many metabolic, endocrine and cardiovascular disorder”
- The G protein-coupled estrogen receptor GPER in health and disease (2011, background): “that are important for maintenance of metabolic function ( Figure 3 )”
- Cytokine and cytokine-like inflammation markers, endothelial dysfunction, and imbalanced coagulation in development of diabetes and its complications. (2009, background): “The concept that heightened inflammation is important in the pathogenesis of T2D (21) is supported by evidence that inflammation in islets, adipose tissue, liver, and muscle may provoke insulin resistance and -cell dysfunction (5, 22, 23) and may therefore antedate the diagnosis of diabetes.”
- Increased Inflammatory Properties of Adipose Tissue Macrophages Recruited During Diet-Induced Obesity (2007, background): “Obesity generates a state of low-grade inflammation that is associated with the development of type 2 diabetes (1).”
- Sterile inflammation: sensing and reacting to damage (2010, background): “, which is increasingly being recognized as having a strong inflammatory componen”
- Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease (2010, positive): “This pathway also plays a critical role in the induction of multiple inflammatory mediators and has been implicated in insulin resistance (Deng et al., 2004; Hu et al., 2006; Shoelson et al., 2006).”
- Upregulated NLRP3 Inflammasome Activation in Patients With Type 2 Diabetes (2012, background): “There is considerable evidence that chronic low-grade inflammation caused by activation of the innate immune system plays an essential role in the pathogenesis of type 2 diabetes and its major complications (3).”
- Association between insulin resistance and the development of cardiovascular disease (2018, background): “These changes may contribute to increased basal lipolysis in obesity and the release of fatty acids into the circulation that consequences a proatherogenic phenotype [19, 90].”
- Obesity induces a phenotypic switch in adipose tissue macrophage polarization. (2007, background): “Introduction Recent investigations suggest that obesity gives rise to a state of chronic, low-grade inflammation that contributes to insulin resistance and type 2 diabetes (1, 2).”
- The Role of Microbial Amino Acid Metabolism in Host Metabolism (2015, background): “Recent work particularly emphasizes the relevance of the innate immune system in the pathogenesis of T2DM [89,90].”