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Liver-specific activation of AMPK prevents steatosis on a high fructose diet

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Title: Liver-specific activation of AMPK prevents steatosis on a high fructose diet
Authors: Carling, D
Woods, A
Williams, JR
Muckett, PJ
Mayer, FV
Liljevald, M
Bohlooly-Y, M
Item Type: Journal Article
Abstract: AMP-activated protein kinase (AMPK) plays a key role in integrating metabolic pathways in response to energy demand. We identified a mutation in the γ1 subunit (γ1D316A) that leads to activation of AMPK. We generated mice with this mutation to study the effect of chronic liver-specific activation of AMPK in vivo. Primary hepatocytes isolated from these mice have reduced gluconeogenesis and fatty acid synthesis, but there is no effect on fatty acid oxidation compared to cells from wild-type mice. Liver-specific activation of AMPK decreases lipogenesis in vivo and completely protects against hepatic steatosis when mice are fed a high-fructose diet. Our findings demonstrate that liver-specific activation of AMPK is sufficient to protect against hepatic triglyceride accumulation, a hallmark of non-alcoholic fatty liver disease (NAFLD). These results emphasize the clinical relevance of activating AMPK in the liver to combat NAFLD and potentially other associated complications (e.g., cirrhosis and hepatocellular carcinoma).
Issue Date: 28-Mar-2017
Date of Acceptance: 1-Mar-2017
URI: http://hdl.handle.net/10044/1/45438
DOI: https://dx.doi.org/10.1016/j.celrep.2017.03.011
ISSN: 2211-1247
Publisher: Elsevier (Cell Press)
Start Page: 3043
End Page: 3051
Journal / Book Title: Cell Reports
Volume: 18
Issue: 13
Copyright Statement: © 2017 The Author(s). This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
Keywords: Science & Technology
Life Sciences & Biomedicine
Cell Biology
FATTY-ACID SYNTHESIS
PROTEIN-KINASE
SKELETAL-MUSCLE
LIPID-METABOLISM
STRUCTURAL BASIS
DISEASE
PHOSPHORYLATION
MICE
HOMEOSTASIS
METFORMIN
AMPK
NAFLD
fructose
lipogenesis
liver disease
steatosis
Publication Status: Published
Appears in Collections:Clinical Sciences
Molecular Sciences
Faculty of Medicine



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