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Inflammation and endoplasmic reticulum stress in obesity and diabetes Hotamisligil GSInt J Obes (Lond) 2008[Dec]; 32 Suppl 7 (Suppl 7): S52-4Obesity is associated with chronic low-grade inflammation. Inflammatory signals interfere with insulin action and disrupt metabolic homeostasis. The c-Jun N-terminal kinase (JNK) has been identified as a central mediator of insulin resistance. Recent studies showed that in obesity compromising endoplasmic reticulum (ER) function results in insulin resistance and type 2 diabetes that are dependent on JNK activation. In contrast, enhancing ER function in transgenic mice or by the use of chemical chaperones protects against diet-induced insulin resistance. Hence, ER stress and the related signaling networks present a critical mechanism underlying obesity-induced JNK activity, inflammatory response and insulin resistance.|Adipose Tissue/enzymology[MESH]|Animals[MESH]|Diabetes Mellitus, Type 2/*physiopathology[MESH]|Endoplasmic Reticulum/enzymology/*physiology[MESH]|Humans[MESH]|Inflammation/*physiopathology[MESH]|Insulin Resistance/*physiology[MESH]|JNK Mitogen-Activated Protein Kinases/genetics/*metabolism[MESH]|Mice[MESH]|Models, Biological[MESH]|Obesity/*physiopathology[MESH]|Protein Folding[MESH]|Stress, Physiological[MESH] |
