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von Loeffelholz, C.* ; Coldewey, S.M.* ; Birkenfeld, A.L.

A narrative review on the role of AMPK on de novo lipogenesis in non-alcoholic fatty liver disease: Evidence from human studies.

Cells 10:1822 (2021)
Publ. Version/Full Text DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
5 ' AMP-activated protein kinase (AMPK) is known as metabolic sensor in mammalian cells that becomes activated by an increasing adenosine monophosphate (AMP)/adenosine triphosphate (ATP) ratio. The heterotrimeric AMPK protein comprises three subunits, each of which has multiple phosphorylation sites, playing an important role in the regulation of essential molecular pathways. By phosphorylation of downstream proteins and modulation of gene transcription AMPK functions as a master switch of energy homeostasis in tissues with high metabolic turnover, such as the liver, skeletal muscle, and adipose tissue. Regulation of AMPK under conditions of chronic caloric oversupply emerged as substantial research target to get deeper insight into the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Evidence supporting the role of AMPK in NAFLD is mainly derived from preclinical cell culture and animal studies. Dysbalanced de novo lipogenesis has been identified as one of the key processes in NAFLD pathogenesis. Thus, the scope of this review is to provide an integrative overview of evidence, in particular from clinical studies and human samples, on the role of AMPK in the regulation of primarily de novo lipogenesis in human NAFLD.
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Publication type Article: Journal article
Document type Review
Corresponding Author
Keywords Lipotoxicity ; Insulin Resistance ; Free Fatty Acids ; Steatohepatitis ; Type 2 Diabetes ; Skeletal Muscle ; Adipose Tissue ; Diacylglycerol; Activated Protein-kinase; Hepatic Insulin-resistance; Human Skeletal-muscle; Intrahepatic Triglyceride Content; Hormone-sensitive Lipase; Adipose-tissue; High-carbohydrate; Follow-up; Glucose-metabolism; Malonyl-coa
ISSN (print) / ISBN 2073-4409
e-ISSN 2073-4409
Journal Cells
Quellenangaben Volume: 10, Issue: 7, Pages: , Article Number: 1822 Supplement: ,
Publisher MDPI
Publishing Place Basel
Non-patent literature Publications
Institute(s) Institute of Diabetes Research and Metabolic Diseases (IDM)