scholarly journals Hepatokines and non-alcoholic fatty liver disease

2016 ◽  
Vol 63 (3) ◽  
Author(s):  
Dariusz M. Lebensztejn ◽  
Marta Flisiak-Jackiewicz ◽  
Irena Białokoz-Kalinowska ◽  
Anna Bobrus-Chociej ◽  
Irina Kowalska
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Growth Factor ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Liver Steatosis ◽  
Visceral Obesity ◽  
Fibroblast Growth Factor 21 ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Nowadays non-alcoholic fatty liver disease (NAFLD) is becoming the most common chronic liver pathology both in adults and children. NAFLD manifestation ranges from a simple liver steatosis to steatohepatitis (nonalcoholic steatohepatitis – NASH), which may progress to advanced fibrosis, cirrhosis and end-stage liver disease. Due to the coexistence of visceral obesity, insulin resistance and dyslipidemia, NAFLD is considered to be the hepatic manifestation of metabolic syndrome. In recent years, in the pathogenesis of metabolic syndrome, type 2 diabetes mellitus, cardiovascular disease and also NAFLD, more and more attention has been paid to the so-called organokines, proteins with both paracrine or/ and endocrine activities. These include most known adipokines (mainly produced by adipose tissue), myokines (mainly produced by skeletal muscles) and hepatokines exclusively or predominantly produced by the liver. It was shown that the liver may affect the lipids and glucose metabolism by hepatokines released into the blood and NAFLD seems to be associated with altered hepatokines production. Fetuin-A, fibroblast growth factor-21 (FGF-21), selenoprotein P, sex hormone-binding globulin (SHBG), angiopoietin-related growth factor (also known as angiopoietin-related protein 6) and leukocyte derived chemotaxin 2 (LECT2) are considered as the most important hepatokines. In this review, we provide an overview of the main hepatokines and we summarize the association of liver-derived proteins with the development and progression of NAFLD.

Fibroblast growth factor 21 in non-alcoholic fatty liver disease

Metabolism ◽  
2019 ◽  
Vol 101 ◽  
pp. 153994 ◽  
Author(s):  
Bradley Tucker ◽  
Huating Li ◽  
Xiaoxue Long ◽  
Kerry-Anne Rye ◽  
Kwok Leung Ong
Keyword(s):  
Liver Disease ◽  
Growth Factor ◽  
Fatty Liver ◽  
Fibroblast Growth Factor ◽  
Fatty Liver Disease ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

552 NON-ALCOHOLIC FATTY LIVER DISEASE AND THE HEPATIC RESPONSE TO SURGERY AMONG PATIENTS WITH ESOPHAGEAL ADENOCARCINOMA

2021 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Noel Donlon ◽  
Jessie A Elliott ◽  
Suzanne L Doyle ◽  
Sinead King ◽  
Peter Beddy ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Esophageal Cancer ◽  
Liver Disease ◽  
Fatty Liver ◽  
Esophageal Adenocarcinoma ◽  
Fatty Liver Disease ◽  
Visceral Obesity ◽  
Oncologic Outcome ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Abstract   Visceral obesity, metabolic syndrome and non-alcoholic fatty liver disease (NAFLD) represent risk factors for esophageal adenocarcinoma (EAC). The prevalence of NAFLD, and its impact on the hepatic response to esophageal cancer surgery, has never been systematically evaluated, and was the focus of this study. Methods Consecutive patients (n = 547) treated with curative intent for esophageal cancer from 2007–2017 were studied. In an unselected subgroup (n = 138), liver biopsies were collected intraoperatively and assessed for NAFLD, defined as ≥5% macrovesicular steatosis. Postoperative complications were recorded prospectively, including Clavien-Dindo grade (CD) and comprehensive complications index (CCI). Liver function tests were monitored in the first postoperative week, with hepatocellular dysfunction defined as a transaminase rise ≥3-times the upper limit of normal. Multivariable logistic and Cox proportional hazards regression were utilised to determine independent predictors of operative and oncologic outcome. The study was registered on clinicaltrials.gov (NCT04152044). Results NAFLD was evident in 62 patients (47.7%) who had biopsies, with a mean (SD) score of 10.1(9.3)%. NAFLD was associated with metabolic syndrome (41.9 vs 25%, P = 0.04), obesity (44.1 vs 11.9%, P < 0.001) and visceral adiposity (172.8 vs 136.5 cm2, P = 0.008), but not clinical or pathologic disease stage. Postoperative hepatocellular dysfunction was observed in 287 (54.8%) patients, associated with NAFLD (P = 0.006), but not visceral obesity (P = 0.396), and normalized in a median (range) of 9 (1–76) days. NAFLD did not impact oncologic outcome, but postoperative hepatocellular dysfunction was independently associated with reduced overall survival (HR 1.87 (1.16–2.29), P = 0.002) on multivariable analysis. Conclusion A marker of metabolic dysregulation in obesity-associated carcinogenesis, NAFLD is prevalent among patients with esophageal cancer. Liver dysfunction post esophagectomy is common, and although temporary, is associated with worse oncologic outcomes. Baseline NAFLD did not incur an adverse long-term oncologic outcome.

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