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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAXESoPcCVM6fAfNw-j1nI3vibBlwTYAMIT3fg8EEAmFw#_5 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAXESoPcCVM6fAfNw-j1nI3vibBlwTYAMIT3fg8EEAmFw#_4 http://www.w3.org/ns/prov#value It seems likely that the inflammatory response is initiated in the adipocytes themselves, as they are the first cells affected by the development of obesity, or potentially in neighboring cells that may be affected by adipose growth. One mechanism that, based on newly emerging data, appears to be of central importance is the activation of inflammatory pathways by ER stress. Obesity generates conditions that increase the demand on the ER (39 41). This is particularly the case for adipose tissue, which undergoes severe changes in tissue architecture, increases in protein and lipid synthesis, and perturbations in intracellular nutrient and energy fluxes. In both cultured cells and whole animals, ER stress leads to activation of JNK and thus contributes to insulin resistance (39). 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