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2016 ; 167
(4
): 1052-1066.e18
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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
PMID27814504
show 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.
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