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The inflammasome puts obesity in the danger zone.

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TLDR
Data suggest that activation of the inflammasome represents a crucial step in the road from obesity to insulin resistance and type 2 diabetes.
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This article is published in Cell Metabolism.The article was published on 2012-01-04 and is currently open access. It has received 238 citations till now. The article focuses on the topics: Inflammasome & Proinflammatory cytokine.

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Citations
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Inflammasomes: mechanism of action, role in disease, and therapeutics

TL;DR: Increasing evidence in mouse models strongly implicates an involvement of the inflammasome in the initiation or progression of diseases with a high impact on public health, such as metabolic disorders and neurodegenerative diseases.
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Probiotics, prebiotics and synbiotics- a review

TL;DR: A comprehensive review on composition and roles of probiotics, prebiotics and synbiotics in human health is presented in this article where additional health benefits like immune-modulation, cancer prevention, inflammatory bowel disease etc. are also discussed.
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Antagonistic crosstalk between NF-κB and SIRT1 in the regulation of inflammation and metabolic disorders.

TL;DR: The molecular mechanisms of the antagonistic signaling between NF-κB and SIRT1 are examined and how this crosstalk controls inflammatory process and energy metabolism is described to induce the appearance of chronic inflammation in metabolic diseases.
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Oxidative Stress in Obesity: A Critical Component in Human Diseases

TL;DR: The aim of this review is to summarize what is known in the relationship between OS in obesity and obesity-related diseases.
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Obesity and cancer risk: Emerging biological mechanisms and perspectives.

TL;DR: How the interplay of these main potential mechanisms and risk factors, exerts their effects on target tissues provoking them to acquire a cancerous phenotype is investigated.
References
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Gout-associated uric acid crystals activate the NALP3 inflammasome

TL;DR: It is shown that MSU and CPPD engage the caspase-1-activating NALP3 (also called cryopyrin) inflammasome, resulting in the production of active interleukin (IL)-1β and IL-18 in mice deficient in the IL-1β receptor.
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Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice

TL;DR: It is found that changes of gut microbiota induced by an antibiotic treatment reduced metabolic endotoxemia and the cecal content of LPS in both high-fat–fed and ob/ob mice, demonstrating that changes in gut microbiota controls metabolic endotoxinemia, inflammation, and associated disorders by a mechanism that could increase intestinal permeability.
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TLR4 links innate immunity and fatty acid–induced insulin resistance

TL;DR: It is suggested that TLR4 is a molecular link among nutrition, lipids, and inflammation and that the innate immune system participates in the regulation of energy balance and insulin resistance in response to changes in the nutritional environment.
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Inflammatory Mechanisms in Obesity

TL;DR: The discovery that obesity itself results in an inflammatory state in metabolic tissues ushered in a research field that examines the inflammatory mechanisms in obesity, and metaflammation is summarized, defined as low-grade, chronic inflammation orchestrated by metabolic cells in response to excess nutrients and energy.
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Type 2 diabetes as an inflammatory disease.

TL;DR: Preliminary results from clinical trials with salicylates and interleukin-1 antagonists support the notion that inflammation participates in the pathogenesis of type 2 diabetes and have opened the door for immunomodulatory strategies for the treatment of T2D that simultaneously lower blood glucose levels and potentially reduce the severity and prevalence of the associated complications of this disease.
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