Inflammation and metabolic disorders

By G. Hotamışlıgil. Nature, 2006

8,992 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/1fda0f889b040edf5ad15501e65d95dd66ca341e

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In Endocrinology, Diabetes and Metabolism

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Citations in the corpus

Defective Hepatic Autophagy in Obesity Promotes ER Stress and Causes Insulin Resistance (2010, background): “The organism cannot adapt and maintain homeostasis under continuous energy and nutrient exposure, and the consequent emergence of metabolic and oxidative stress leads to inflammation responses and organelle dysfunction (Hotamisligil, 2006, 2010).”
Added Sugar Intake and Cardiovascular Diseases Mortality Among US Adults (2014, neutral): “The number needed to harm at 15 years of follow-up (median follow-up) reduced from 265 (95% CI, 166-715) to 22 (13-66) (Table 2).”
Adipocyte-derived Th2 cytokines and myeloid PPARdelta regulate macrophage polarization and insulin sensitivity. (2008, background): “At the signaling level, inflammatory and metabolic processes are intertwined and integral components of metabolic diseases (Hotamisligil, 2006).”
Regulatory Mechanisms for Adipose Tissue M1 and M2 Macrophages in Diet-Induced Obese Mice (2009, background): “3 besity and insulin resistance are closely associated with a state of low-grade inflammation in adipose tissue, where resident macrophages play important roles (1-9).”
CD8+ effector T cells contribute to macrophage recruitment and adipose tissue inflammation in obesity (2009, background): “1964" language="eng" relation="no"> Inflammation is now considered to have a pivotal role in the development of metabolic disease”
High Fat Diet-Induced Gut Microbiota Exacerbates Inflammation and Obesity in Mice via the TLR4 Signaling Pathway (2012, background): “Nowadays, it is widely accepted that metabolic syndrome is associated with low-grade systemic inflammation, despite the fact that the molecular origin of the inflammation is unknown [2,3].”
iArc monogrAphs on the evAluAtion oF cArcinogenic risks to humAns (2012, background): “In NAFLD, chronic excess of nutrients causes endoplasmic reticulum stress, and leads to an increase of hepatic fat (steatosis) and insulin resistance; a complex interplay between these factors can lead to chronic liver inflammation, apoptosis and fibrogenesis, which are thought to form the prelude t”
The Inflammasome-Mediated Caspase-1 Activation Controls Adipocyte Differentiation and Insulin Sensitivity (2010, background): “In addition to adipocyte hypertrophy due to storage of increasing amounts of lipids, adipose tissue turns into an inflamed tissue characterized by macrophage infiltration and altered secretion of adipokines (Hotamisligil, 2006; Weisberg et al., 2003).”
Proteobacteria: A Common Factor in Human Diseases (2017, background): “A connection between low-grade inflammation, sustained by lipopolysaccharides (LPS), and the development of metabolic disorders is well established [26]; however the hypothesis regarding the direct role of the microbiota in the development of this inflammatory state, called endotoxemia, is more rece”
The interaction of hepatic lipid and glucose metabolism in liver diseases. (2012, background): “Obesity increases the TNFa production in adipocytes, which facilitates adipocyte IR and increases lipolysis rate [82].”
The role of the gut microbiota in energy metabolism and metabolic disease. (2009, background): “Although all these elegant studies revealed that the gut microbiota exerts a crucial role in the development of adiposity and the regulation of homeostasis, it remains to be demonstrated how the gut microbiota can be involved in the development of a low-grade inflammation classically associated with”
The role of exercise and PGC1α in inflammation and chronic disease (2008, background): “For example, the infiltration of immune cells into white adipose tissue, and therefore inflammation in this tissue, is closely correlated with the development of insulin resistance and type 2 diabete”