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10.1016/j.celrep.2017.03.011

http://scihub22266oqcxt.onion/10.1016/j.celrep.2017.03.011
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C5382239!5382239!28355557
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suck abstract from ncbi


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pmid28355557      Cell+Rep 2017 ; 18 (13): 3043-51
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  • Liver-Specific Activation of AMPK Prevents Steatosis on a High-Fructose Diet #MMPMID28355557
  • Woods A; Williams JR; Muckett PJ; Mayer FV; Liljevald M; Bohlooly-Y M; Carling D
  • Cell Rep 2017[Mar]; 18 (13): 3043-51 PMID28355557show ga
  • AMP-activated protein kinase (AMPK) plays a key role in integrating metabolic pathways in response to energy demand. We identified a mutation in the ?1 subunit (?1D316A) 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).
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