Inflammation, stress, and diabetes.

By K. Wellen, G. Hotamisligil. Journal of Clinical Investigation, 2005

4,215 citations recorded by the source corpus.

Subfields: Epidemiology, Genetics, Physiology

View Paper: https://www.semanticscholar.org/paper/19a68b23ff2165ea3c43fba9f6163d06469f628e

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Citations in the corpus

Adverse effects of the classic antioxidant uric acid in adipocytes: NADPH oxidase-mediated oxidative/nitrosative stress. (2007, background): “Oxidative stress and inflammation in the adipose tissue induce an imbalance in the production of adipocyte-specific hormones and cytokines (adipokines) that contribute substantially to the development of insulin resistance and cardiovascular risk associated with obesity (6, 13, 57).”
Plasma Ceramides Are Elevated in Obese Subjects With Type 2 Diabetes and Correlate With the Severity of Insulin Resistance (2009, background): “Diabetes 58:337–343, 2009 Type 2 diabetes is an insulin-resistant state characterized by impaired glucose tolerance (1) and inflammation (2).”
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: From Mechanisms to Therapeutic Strategies (2021, background): “Inflammation Systemic chronic inflammatory response characterized by altered cytokine production and the activations of inflammatory signaling pathways is being actively investigated to determine its role in obesity-related insulin resistance [145].”
Hepatocyte-specific Deletion of SIRT1 Alters Fatty Acid Metabolism and Results in Hepatic Steatosis and Inflammation (2009, background): “Since bothER stress and inflammation directly contribute to the development of insulin resistance (Wellen and Hotamisligil, 2005), 334 Cell Metabolism 9, 327–338, April 8, 2009 ª2009 Elsevier Inc. our observations imply that SIRT1 LKO mice would show signs of altered insulin signaling.”
Inflammation and metabolic disorders (2006, background): “Key conceptual considerations During the past decade, it became clear that inflammation is a key feature of obesity and type 2 diabete”
Leptin and Obesity: Role and Clinical Implication (2021, background): “These feedback loops explain why obesity is associated with chronic proinflammatory signaling pathways, abnormal cytokine production, and increased acute-phase reactants (80) and why obesity increases an individual’s risk of developing inflammatory-based diseases and immune-mediated disorders (80–82”