Obesity-induced inflammatory changes in adipose tissue.

By K. Wellen, G. Hotamisligil. Journal of Clinical Investigation, 2003

1,896 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/607ed2c0cff2b0c555a22f1a51de4f05ca27fe6b

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Citations in the corpus

Recent advances in the relationship between obesity, inflammation, and insulin resistance. (2006, background): “This increase in macrophage infiltration could represent the cause and/or the consequence of the low-grade inflammation state associated with obesity [41, 42].”
Insulin resistance, lipotoxicity, type 2 diabetes and atherosclerosis: the missing links. The Claude Bernard Lecture 2009 (2010, background): “Adipose tissue of obese and type 2 diabetic individuals is infiltrated by mononuclear cells and is in a state of chronic inflammation [167].”
Gut microorganisms, mammalian metabolism and personalized health care (2005, background): “Although speculative, the global importance of this problem warrants further investigation into the role of altered gut microorganisms in insulin resistance, diabetes and obesity, especially considering the well known chronic gut inflammatory changes that are linked to obesity and type II diabete”
Effects of obesity on bone metabolism (2011, background): “Fourth, both obesity and osteoporosis are associated with elevated oxidative stress and increased production of proinflammatory cytokines [19,20].”
Immune System to Brain Signaling: Neuropsychopharmacological Implications (2011, background): “…a chronic condition which is associated with low-grade inflammatory processes, with increased circulating levels of acute phase proteins (CRP in particular) and pro-inflammatory cytokines being observed in both adult and younger obese subjects (Bastard et al., 1999; Wellen and Hotamisligil, 2003).”
Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans Published, JLR Papers in Press, September 8, 2005. DOI 10.1194/jlr.M500294-JLR200 (2005, background): “event in the development of obesity complications, especially type 2 diabetes (1-7).”
Reduction of macrophage infiltration and chemoattractant gene expression changes in white adipose tissue of morbidly obese subjects after surgery-induced weight loss. (2005, background): “Macrophage infiltration in WAT may be both a cause and a consequence of the local and chronic inflammatory status in obesity (15).”
Obesity in pregnancy stimulates macrophage accumulation and inflammation in the placenta. (2008, background): “Infiltration of vascularized tissues or organs by circulating monocytes is considered a general mechanism to cope with systemic inflammation [38,39].”
Adipocyte dysfunctions linking obesity to insulin resistance and type 2 diabetes (2008, background): “Secreted TNFα by macrophages and adipocytes within the adipose tissue of obese humans and animal”