Nutrient sensing and inflammation in metabolic diseases

By G. Hotamışlıgil, Ebru Erbay. Nature reviews. Immunology, 2008

1,054 citations recorded by the source corpus.

The proper functioning of the pathways that are involved in the sensing and management of nutrients is central to metabolic homeostasis and is therefore among the most fundamental requirements for survival. Metabolic systems are integrated with pathogen-sensing and immune responses, and these pathways are evolutionarily conserved. This close functional and molecular integration of the immune and metabolic systems is emerging as a crucial homeostatic mechanism, the dysfunction of which underlies many chronic metabolic diseases, including type 2 diabetes and atherosclerosis. In this Review we provide an overview of several important networks that sense and manage nutrients and discuss how they integrate with immune and inflammatory pathways to influence the physiological and pathological metabolic states in the body.

Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/2b709117a6df57d16f49628622b4b9946bd25aee

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Citations in the corpus

Inflammasome is a central player in the induction of obesity and insulin resistance (2011, background): “To date, several proinflammatory cytokines have been linked to the development of insulin resistance, including IL-1β and IL-18 (14).”
Transcriptional control of adipose lipid handling by IRF4 (2011, background): “The recent realization that obesity represents a state of chronic inflammation has led to the identification of many genes and proteins, previously thought to act specifically on immune function, as key regulators of metabolism (Hotamisligil and Erbay, 2008).”
The NALP3/NLRP3 Inflammasome Instigates Obesity-Induced Autoinflammation and Insulin Resistance (2011, background): “2279" language="eng" relation="no"> Despite the absence of any overt infection or definitive evidence of autoantigen-mediated immune cell activation during obesity, chronic inflammation in this state is an established instigator of several diseases such as type 2 diabetes, defective immunit”
Metabolic dysfunction drives a mechanistically distinct proinflammatory phenotype in adipose tissue macrophages. (2014, background): “…marker expression by proinflammatory ATMs in obese humans and mice suggested that distinct pathways might promote macrophage inflammation in the context of obesity, a hypothesis that has been proposed by Hotamisligil and colleagues (Calay and Hotamisligil, 2013; Hotamisligil and Erbay, 2008).”
Omega-3 fatty acids prevent inflammation and metabolic disorder through inhibition of NLRP3 inflammasome activation. (2013, background): “It is noteworthy that each of these cellular stresses is also thought to elicit or associate with inflammatory response (Hotamisligil and Erbay, 2008; Masters et al., 2010).”
The endocannabinoid system links gut microbiota to adipogenesis (2010, background): “Recent data have shown that these metabolic disorders are characterised by low-grade inflammation of unknown molecular origin (Hotamisligil and Erbay, 2008; Shoelson and Goldfine, 2009); therefore, it is of the utmost importance to identify the link between inflammation and adipose tissue…”