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Text
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<a href="http://doi.org/10.1016/j.molmet.2017.08.011" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.molmet.2017.08.011</a>
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Pages
1517-1528
Issue
11
Volume
6
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Title
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Decreasing Cb1 Receptor Signaling In Kupffer Cells Improves Insulin Sensitivity In Obese Mice
Publisher
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Molecular Metabolism
Date
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2017
2017-11
Subject
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adiponectin receptors; adipose-tissue; CB1 receptors; disruption; endocannabinoid system; Endocrinology & Metabolism; fatty liver-disease; Inflammation; Insulin resistance; Kupffer cells; macrophage polarization; nf-kappa-b; nonalcoholic steatohepatitis; protein-2; reactive oxygen; siRNA; targeted; uncoupling
Creator
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Jourdan T; Nicoloro S M; Zhou Z; Shen Y F; Liu J; Coffey N J; Cinar R; Godlewski G; Gao B; Aouadi M; Czech M P; Kunos G
Description
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Objective: Obesity-induced accumulation of ectopic fat in the liver is thought to contribute to the development of insulin resistance, and increased activity of hepatic CB1R has been shown to promote both processes. However, lipid accumulation in liver can be experimentally dissociated from insulin resistance under certain conditions, suggesting the involvement of additional mechanisms. Obesity is also associated with pro-inflammatory changes which, in turn, can promote insulin resistance. Kupffer cells (KCs), the liver's resident macrophages, are the major source of pro-inflammatory cytokines in the liver, such as TNF-alpha, which has been shown to inhibit insulin signaling in multiple cell types, including hepatocytes. Here, we sought to identify the role of CB1R in KCs in obesity-induced hepatic insulin resistance. Methods: We used intravenously administered beta-D-glucan-encapsulated siRNA to knock-down CB1R gene expression selectively in KCs. Results: We demonstrate that a robust knock-down of the expression of Cnr1, the gene encoding CB1R, results in improved glucose tolerance and insulin sensitivity in diet-induced obese mice, without affecting hepatic lipid content or body weight. Moreover, Cnr1 knock-down in KCs was associated with a shift from pro-inflammatory M1 to anti-inflammatory M2 cytokine profile and improved insulin signaling as reflected by increased insulin-induced Akt phosphorylation. Conclusion: These findings suggest that CB1R expressed in KCs plays a critical role in obesity-related hepatic insulin resistance via a pro inflammatory mechanism. Published by Elsevier GmbH.
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<a href="http://doi.org/10.1016/j.molmet.2017.08.011" target="_blank" rel="noreferrer noopener">10.1016/j.molmet.2017.08.011</a>
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Journal Article or Conference Abstract Publication
2017
adiponectin receptors
adipose-tissue
Aouadi M
cb1 receptors
Cinar R
Coffey N J
Czech M P
disruption
endocannabinoid system
Endocrinology & Metabolism
fatty liver-disease
Gao B
Godlewski G
Inflammation
Insulin Resistance
Jourdan T
Journal Article or Conference Abstract Publication
Kunos G
Kupffer cells
Liu J
macrophage polarization
Molecular metabolism
nf-kappa-b
Nicoloro S M
Nonalcoholic steatohepatitis
protein-2
Reactive oxygen
Shen Y F
siRNA
targeted
uncoupling
Zhou Z