De novo non-alcoholic fatty liver disease after liver transplantation – as diagnosed by magnetic resonance

2020 ◽  
pp. 116-122
Author(s):  
Ľubomír Skladaný ◽  
Svetlana Adamcová-Selčanov ◽  
Stanislava Čiefová ◽  
Natalia Bystrianska ◽  
Beata Škvarková ◽  
...  
2003 ◽  
Vol 3 (11) ◽  
pp. 1413-1417 ◽  
Author(s):  
Fred Poordad ◽  
Robert Gish ◽  
Adil Wakil ◽  
Richard Garcia-Kennedy ◽  
Paul Martin ◽  
...  

2020 ◽  
Vol 104 (S3) ◽  
pp. S487-S488
Author(s):  
Lubomir Skladany ◽  
Svetlana Adamcova Selcanova ◽  
Jana Ciefova ◽  
Natalia Bystrianska ◽  
Beata Skvarkova ◽  
...  

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1822
Author(s):  
Christian von Loeffelholz ◽  
Sina M. Coldewey ◽  
Andreas L. Birkenfeld

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.


2022 ◽  
Vol 8 ◽  
Author(s):  
Speranta Iacob ◽  
Susanne Beckebaum ◽  
Razvan Iacob ◽  
Cristian Gheorghe ◽  
Vito Cicinnati ◽  
...  

Recurrent or de novo non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH) following liver transplantation (LT) is a frequent event being increasingly recognized over the last decade, but the influence of recurrent NASH on graft and patient outcomes is not yet established. Taking into consideration the long term survival of liver transplanted patients and long term complications with associated morbidity and mortality, it is important to define and minimize risk factors for recurrent NAFLD/NASH. Metabolic syndrome, obesity, dyslipidemia, diabetes mellitus are life style risk factors that can be potentially modified by various interventions and thus, decrease the risk of recurrent NAFLD/NASH. On the other hand, genetic factors like recipient and/or donor PNPLA3, TM6SF2, GCKR, MBOAT7 or ADIPOQ gene polymorphisms proved to be risk factors for recurrent NASH. Personalized interventions to influence the different metabolic disorders occurring after LT in order to minimize the risks, as well as genetic screening of donors and recipients should be performed pre-LT in order to achieve diagnosis and treatment as early as possible.


PLoS ONE ◽  
2019 ◽  
Vol 14 (11) ◽  
pp. e0224820 ◽  
Author(s):  
Denisa Erhartova ◽  
Monika Cahova ◽  
Helena Dankova ◽  
Marie Heczkova ◽  
Irena Mikova ◽  
...  

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