Obesity, inflammation, and insulin resistance.

By S. Shoelson, Laura Herrero, A. Naaz. Gastroenterology, 2007

1,843 citations recorded by the source corpus.

Subfields: Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/a320c175d551ac7e09700f50fe2c166c994478d6

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. Jerrold M. Olefsky
2. Christopher D. Byrne
3. Christopher K. Glass
4. G. Targher
5. M. Karin
6. Brandon H Hidaka
7. S. Caldwell
8. Charles L Raison

In Physiology

1. Jerrold M. Olefsky
2. Vickie E. Baracos
3. K. Fearon
4. R. Zechner
5. M. Karin
6. Christopher D. Byrne
7. Christopher K. Glass
8. Charles L Raison

Citations in the corpus

• Effects of obesity on bone metabolism (2011, neutral): “progression of obesity-related health disorders [31].”
• INFLAMMATION AND LIPID SIGNALING IN THE ETIOLOGY OF INSULIN RESISTANCE (2012, positive): “The etiology of insulin resistance has been intensely studied (Qatanani and Lazar, 2007; Shulman, 2000), and it is now recognized that chronic tissue inflammation is an important cause of obesity-induced insulin resistance (Attie and Scherer, 2009; Lumeng and Saltiel, 2011; Olefsky and Glass, 2010; ”
• Weight loss and lipolysis promote a dynamic immune response in murine adipose tissue. (2010, background): “During weight gain and in cross-sectional studies of weight-stable humans, there is a positive, nearly linear relationship between adiposity and markers of local and systemic inflammation (13).”
• GPR120 is an omega-3 fatty acid receptor mediating potent anti-inflammatory and insulin-sensitizing effects. (2010, positive): “Since chronic tissue inflammation is an important mechanism causing insulin resistance (Xu et al., 2003; Shoelson et al., 2007; Schenk et al., 2008), the anti-inflammatory actions of u-3 FAs exert potent insulin sensitizing effects.”
• Dietary and genetic obesity promote liver inflammation and tumorigenesis by enhancing IL-6 and TNF expression (2010, background): “Furthermore, inactivation of TNFR1, a receptor whose Cell 140, 197–208 lipid accumulation (Arkan et al., 2005; Hotamisligil, 2006; Shoelson et al., 2007; Solinas et al., 2007).”
• NAFLD: a multisystem disease. (2015, background): “atherogenesis and in the development of insulin resistance and NAFLD [54,58,71,72,75,143–145].”