Inflammation and activated innate immunity in the pathogenesis of type 2 diabetes.
By J. Pickup. Diabetes Care, 2004
1,504 citations recorded by the source corpus.
Subfields: Epidemiology, Genetics, Immunology
View Paper: https://www.semanticscholar.org/paper/4daf2b76615f4673d5a25fd5a5f23f0a468bc1e7
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Epidemiology
- Joel T. Dudley
- Atul J. Butte
- Euan A. Ashley
- Julian P. T. Higgins
- G. Hotamisligil
- K. Wellen
- B. Wajchenberg
- Mitchell A. Lazar
In Genetics
- Teri E. Klein
- Joel T. Dudley
- M. Blasco
- Hua Tang
- Russ B. Altman
- Atul J. Butte
- Mark Gerstein
- Konrad J. Karczewski
In Immunology
Citations in the corpus
- Long-Term Interleukin-6 Levels and Subsequent Risk of Coronary Heart Disease: Two New Prospective Studies and a Systematic Review (2008, background): “There are moderate associations of IL-6 levels with some established risk factors (notably smoking, diabetes, and dyslipidemia) and with several downstream inflammatory markers, consistent with the key role of IL-6 in mediating inflammatory cascades [3–5,41–44].”
- Oxidative Stress in Obesity: A Critical Component in Human Diseases (2014, background): “that subclinical systemic inflammation in obese patients, as measured by elevated levels of CRP, IL-6, and TNF-α, predicts the development of type 2 diabetes [87,88] and contributes to a decrease of insulin sensitivity in peripheral tissues [89].”
- Personal Omics Profiling Reveals Dynamic Molecular and Medical Phenotypes (2012, background): “This analysis revealed a modest elevated risk for coronary artery disease and significantly elevated risk levels of basal cell carcinoma (Figure 2B), hypertriglyceridemia, and type 2 diabetes (T2D) (Figures 2B and 2C).”
- beta-cell failure in diabetes and preservation by clinical treatment. (2007, background): “In addition to the endocrine activity of the adipocytes, described above, macrophages and endothelium may contribute to increasing serum levels of IL-1 , IL-6, and TNF- in DM2 (71) and may act on the pancreatic islets and impair -cell secretory function or activate the innate immune system (67).”
- Glycogen Synthase Kinase-3 (GSK3): Inflammation, Diseases, and Therapeutics (2007, background): “TNF and IL-6 represent only two examples of numerous inflammatory molecules for which elevations have been linked to the development of type 2 diabetes, and several anti-inflammatory drugs have been reported to decrease the risk of developing type 2 diabetes [150].”
- AMPK, insulin resistance, and the metabolic syndrome. (2013, neutral): “drome typically have a decreased capacity for exercise (28) and show evidence of low-grade inflammation (29), similar to patients with obesity and type 2 diabetes (24, 29).”
- Burnout and risk of cardiovascular disease: evidence, possible causal paths, and promising research directions. (2006, background): “Recent studies provide evidence indicating a link between inflammation, atherosclerosis, and CVD (Hansson, 2005; Koenig, 2001; Libby, Ridker, & Maseri, 2002; Ross, 1999) and the pathogenesis of Type 2 diabetes (Pickup, 2004).”
- Inflammation, stress, and diabetes. (2005, positive): “…became clear, however, that obesity is characterized by a broad inflammatory response and that many inflammatory mediators exhibit patterns of expression and/or impact insulin action in a manner similar to that of TNF-α during obesity, in animals ranging from mice and cats to humans (12–14).”