Results 41 to 50 of about 236,526 (353)

Pediatric non alcoholic fatty liver disease: old and new concepts on development, progression, metabolic insight and potential treatment targets [PDF]

, 2013
Nonalcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease in children. NAFLD has emerged to be extremely prevalent, and predicted by obesity and male gender.
Giorgio V, Graziano F, Nobili V., Prono F   +3 more
core   +1 more source

Relationship between Controlled Attenuation Parameter and Hepatic Steatosis as Assessed by Ultrasound in Alcoholic or Nonalcoholic Fatty Liver Disease

Gut and Liver, 2016
Background/Aims : The aim of this study was to evaluate the relationship between controlled attenuation parameter (CAP) and hepatic steatosis, as assessed by ultrasound (US) in patients with alcoholic liver disease (ALD) or non-alcoholic fatty liver ...
doaj   +1 more source

Discriminating Different Classes of Toxicants by Transcript Profiling [PDF]

, 2004
Male rats were treated with various model compounds or the appropriate vehicle controls. Most substances were either well-known hepatotoxicants or showed hepatotoxicity during preclinical testing.
Albertini, Silvio, Boess, Franziska, de Vera, Maria Cristina, Gasser, Rodolfo, Ruepp, Stefan, Steiner, Guido, Suter, Laura   +6 more
core   +2 more sources

Accumulation of PNPLA3 on lipid droplets is the basis of associated hepatic steatosis

Proceedings of the National Academy of Sciences of the United States of America, 2019
Significance A sequence variant (I148M) in PNPLA3 is a major genetic risk factor for nonalcoholic fatty liver disease. Previously, we showed that PNPLA3(148M) evades ubiquitylation-mediated degradation and accumulates to high levels on lipid droplets ...
Soumik Basuray, Yang Wang, E. Smagris, Jonathan C. Cohen, H. Hobbs   +4 more
semanticscholar   +1 more source

Neutral Sphingomyelinase 2 Inhibition Limits Hepatic Steatosis and Inflammation

Cells
Non-alcoholic fatty liver disease (NAFLD) is manifested by hepatic steatosis, insulin resistance, hepatocyte death, and systemic inflammation. Obesity induces steatosis and chronic inflammation in the liver.
Fatema Al-Rashed, Hossein Arefanian, Ashraf Al Madhoun, Fatemah Bahman, Sardar Sindhu, Halemah AlSaeed, Texy Jacob, Reeby Thomas, Areej Al-Roub, Fawaz Alzaid, MD Zubbair Malik, Rasheeba Nizam, Thangavel Alphonse Thanaraj, Fahd Al-Mulla, Yusuf A. Hannun, Rasheed Ahmad   +15 more
doaj   +1 more source

Prenatal hyperandrogenism induces alterations that affect liver lipid metabolism [PDF]

, 2016
Prenatal hyperandrogenism is hypothesized as one of the main factors contributing to26 the development of polycystic ovary syndrome (PCOS). PCOS patients have high risk27 of developing fatty liver and steatosis.
Abruzzese, Giselle Adriana, Ferreira, Silvana Rocío, Heber, María Florencia, Motta, Alicia Beatriz, Pignataro, Omar Pedro, Reynoso, Roxana María, Velez, Leandro Martin   +6 more
core   +2 more sources

Normalization of Oxygen Levels Induces a Metabolic Reprogramming in Livers Exposed to Intermittent Hypoxia Mimicking Obstructive Sleep Apnea

Antioxidants
Obstructive sleep apnea (OSA), characterized by intermittent hypoxia (IH), is strongly associated with metabolic syndrome and metabolic dysfunction-associated steatotic liver disease (MASLD).
Miguel Á. Hernández-García, Beatriz Aldave-Orzáiz, Carlos Ernesto Fernández-García, Esther Fuertes-Yebra, Esther Rey, Ángela Berlana, Ramón Farré, Carmelo García-Monzón, Isaac Almendros, Pedro Landete, Águeda González-Rodríguez   +10 more
doaj   +1 more source

Liver transplantation for alcoholic cirrhosis: Long term follow-up and impact of disease recurrence [PDF]

, 2001
Background. Alcoholic liver disease has emerged as a leading indication for hepatic transplantation, although it is a controversial use of resources. We aimed to examine all aspects of liver transplantation associated with alcohol abuse.
Andrea M. DiMartini, Anthony J. Demetris, Ashok Jain, Balan, Bassendine, Becker, Belle, Bellentani, Beresford, Beresford, Beresford, Berlakovich, Bernard, Bizollon, Blakolmer, Campbell, Chao, Christopher O.C. Bellamy, Conjeevaram, Cromie, Duvoux, Enomoto, Everhart, Everson, Fauerholdt, Ferrell, Forrest Dodson, Foster, Gane, Graziadei, Harrison, Hoofnagle, Howard, Iezzoni, Ishak, Jain, John J. Fung, Keeffe, Kenngott, Kris Ruppert, Kumar, Kyriacou, Lee, Levin, Levy, Lucey, Lucey, Lucey, Mendenhall, Michael Torbenson, Nabel, Neuberger, Neuberger, Neuberger, Osorio, Pageaux, Pappo, Pereira, Reed, Reich, Saunders, Schiff, Seitz, Sherlock, Shev, Starzl, Tang, Thomas E. Starzl, Tringali, Uchimura, Wiesner, Yates   +71 more
core   +1 more source

GSH Attenuates Organ Injury and Improves Function after Transplantation of Fatty Livers [PDF]

, 2010
Ischemia-reperfusion injury (IRI) is increased after transplantation of steatotic livers. Since those livers are increasingly used for transplantation, protective strategies must be developed. Reactive oxygen species (ROS) play a key role in hepatic IRI.
Angele, M. K., Bilzer, M., Gruetzner, U., Jauch, Karl-Walter, Löhe, F., Pratschke, S., Schauer, R. J., Tufman, A.   +7 more
core   +1 more source

Imeglimin attenuates liver fibrosis by inhibiting vesicular ATP release from hepatic stellate cells

FEBS Letters, EarlyView.
Imeglimin, at clinically relevant concentrations, inhibits vesicular ATP accumulation and release from hepatic stellate cells, thereby attenuating purinergic signaling and reducing fibrogenic activation. This mechanism reveals a newly identified antifibrotic action of imeglimin beyond glycemic control.
Seiji Nomura, Lixiang Wang, Nao Hasuzawa, Ayako Nagayama, Sawako Moriyama, Kenji Ashida, Yoshinori Moriyama, Masatoshi Nomura, Ken Yamamoto   +8 more
wiley   +1 more source