Imperial College London


Faculty of MedicineInstitute of Clinical Sciences

Professor of Biochemistry



+44 (0)20 3313 4313david.carling




3rd Fl CRBHammersmith HospitalHammersmith Campus






BibTex format

author = {Carling, D and Woods, A and Williams, JR and Muckett, PJ and Mayer, FV and Liljevald, M and Bohlooly-Y, M},
doi = {10.1016/j.celrep.2017.03.011},
journal = {Cell Reports},
pages = {3043--3051},
title = {Liver-specific activation of AMPK prevents steatosis on a high fructose diet},
url = {},
volume = {18},
year = {2017}

RIS format (EndNote, RefMan)

AB - 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).
AU - Carling,D
AU - Woods,A
AU - Williams,JR
AU - Muckett,PJ
AU - Mayer,FV
AU - Liljevald,M
AU - Bohlooly-Y,M
DO - 10.1016/j.celrep.2017.03.011
EP - 3051
PY - 2017///
SN - 2211-1247
SP - 3043
TI - Liver-specific activation of AMPK prevents steatosis on a high fructose diet
T2 - Cell Reports
UR -
UR -
VL - 18
ER -