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10.1016/j.cell.2016.10.015 http://scihub22266oqcxt.onion/10.1016/j.cell.2016.10.015 C5908236!5908236!27814504     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell 2016 ; 167 (4): 1052-1066.e18 Nephropedia Template TP {{tp|p=27814504|t=2016. Inflammation Improves Glucose Homeostasis Through IKK?-XBP1s Interaction |pdf=|usr=}}{{27814504}} gab.com Text Inflammation Improves Glucose Homeostasis Through IKK -XBP1s Interaction JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=27814504 #FOAvip It is widely believed that inflammation associated with obesity has an important role in the development of type 2 diabetes. I?B kinase beta (IKK?) is a crucial kinase that responds to inflammatory stimuli such as Tumor Necrosis Factor ? (TNF?), by initiating a variety of intracellular signaling cascades, and is considered to be a key element in the inflammation-mediated development of insulin resistance. We show here, contrary to expectation, that IKK?-mediated inflammation is a positive regulator of hepatic glucose homeostasis. IKK? phosphorylates the spliced form of X-Box Binding Protein 1 (XBP1s) and increases the activity of XBP1s. We have used three experimental approaches to enhance the IKK? activity in the liver of obese mice, and observed increased XBP1s activity, reduced ER stress, and a significant improvement in insulin sensitivity and consequently in glucose homeostasis. Our results reveal a beneficial role of IKK?-mediated hepatic inflammation in glucose homeostasis. Twit Text FOAVip Inflammation Improves Glucose Homeostasis Through IKK -XBP1s Interaction ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=27814504 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27814504 #FOAvip English Wikipedia <ref>{{Cite pmid|27814504}}</ref> Inflammation Improves Glucose Homeostasis Through IKK?-XBP1s Interaction #MMPMID27814504 Liu J; Ibi D; Taniguchi K; Lee J; Herrema H; Akosman B; Mucka P; Salazar Hernandez MA; Uyar MF; Park SW; Karin M; Ozcan U Cell 2016[Nov]; 167 (4): 1052-1066.e18 PMID27814504show ga It is widely believed that inflammation associated with obesity has an important role in the development of type 2 diabetes. I?B kinase beta (IKK?) is a crucial kinase that responds to inflammatory stimuli such as Tumor Necrosis Factor ? (TNF?), by initiating a variety of intracellular signaling cascades, and is considered to be a key element in the inflammation-mediated development of insulin resistance. We show here, contrary to expectation, that IKK?-mediated inflammation is a positive regulator of hepatic glucose homeostasis. IKK? phosphorylates the spliced form of X-Box Binding Protein 1 (XBP1s) and increases the activity of XBP1s. We have used three experimental approaches to enhance the IKK? activity in the liver of obese mice, and observed increased XBP1s activity, reduced ER stress, and a significant improvement in insulin sensitivity and consequently in glucose homeostasis. Our results reveal a beneficial role of IKK?-mediated hepatic inflammation in glucose homeostasis. äInflammation Improves Glucose Homeostasis Through IKK?-XBP1s Interacti(epmc).pdf DeepDyve Pubget Overpricing