scholarly journals Prospective Investigation of Serum Metabolites, Coffee Drinking, Liver Cancer Incidence, and Liver Disease Mortality

2019 ◽  
Vol 112 (3) ◽  
pp. 286-294 ◽  
Author(s):  
Erikka Loftfield ◽  
Joseph A Rothwell ◽  
Rashmi Sinha ◽  
Pekka Keski-Rahkonen ◽  
Nivonirina Robinot ◽  
...  

Abstract Background Coffee has been consistently associated with lower risk of liver cancer and chronic liver disease, suggesting that coffee affects mechanisms underlying disease development. Methods We measured serum metabolites using untargeted metabolomics in 1:1 matched nested case-control studies of liver cancer (n = 221 cases) and fatal liver disease (n = 242 cases) in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention cohort (n = 29 133). Associations between baseline coffee drinking and metabolites were identified using linear regression; conditional logistic regression models were used to identify associations with subsequent outcomes. Results Overall, 21 metabolites were associated with coffee drinking and also each subsequent endpoint; nine metabolites and trigonelline, a known coffee biomarker, were identified. Tyrosine and two bile acids, glycochenodeoxycholic acid (GCDCA) and glycocholic acid (GCA), were inversely associated with coffee but positively associated with both outcomes; odds ratios (ORs) comparing the 90th to 10th percentile (modeled on a continuous basis) ranged from 3.93 (95% confidence interval [CI] = 2.00 to 7.74) for tyrosine to 4.95 (95% CI = 2.64 to 9.29) for GCA and from 4.00 (95% CI = 2.42 to 6.62) for GCA to 6.77 (95% CI = 3.62 to 12.65) for GCDCA for liver cancer and fatal liver disease, respectively. The remaining six metabolites and trigonelline were positively associated with coffee drinking but inversely associated with both outcomes; odds ratio ranged from 0.16 to 0.37. Associations persisted following diet adjustment and for outcomes occurring greater than 10 years after blood collection. Conclusions A broad range of compounds were associated with coffee drinking, incident liver cancer, and liver disease death over 27 years of follow-up. These associations provide novel insight into chronic liver disease and liver cancer etiology and support a possible hepatoprotective effect of coffee.

PLoS ONE ◽  
2018 ◽  
Vol 13 (9) ◽  
pp. e0203926 ◽  
Author(s):  
Jake E. Thistle ◽  
Baiyu Yang ◽  
Jessica L. Petrick ◽  
Jin-Hu Fan ◽  
You-Lin Qiao ◽  
...  

2013 ◽  
Author(s):  
Gabriel Y. Lai ◽  
Stephanie J. Weinstein ◽  
Demetrius Albanes ◽  
Philip R. Taylor ◽  
Katherine A. McGlynn ◽  
...  

2017 ◽  
Author(s):  
Baiyu Yang ◽  
Jessica L. Petrick ◽  
Christian C. Abnet ◽  
Barry I. Graubard ◽  
Stephanie J. Weinstein ◽  
...  

2006 ◽  
Vol 36 ◽  
pp. S206
Author(s):  
A.P. Ortiz ◽  
C. Pérez ◽  
C.J. Romero ◽  
O. Disdier ◽  
E. Santana ◽  
...  

2003 ◽  
Vol 104 (3) ◽  
pp. 310-317 ◽  
Author(s):  
Laura Silvestri ◽  
Laura Sonzogni ◽  
Annalisa De Silvestri ◽  
Chiara Gritti ◽  
Luciana Foti ◽  
...  

2020 ◽  
Vol 52 (10) ◽  
pp. 1766-1776
Author(s):  
Min Kim ◽  
Changhu Lee ◽  
Dae Yun Seo ◽  
Hyojung Lee ◽  
Jay D. Horton ◽  
...  

Abstract Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease and can lead to multiple complications, including non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma. The fibrotic liver is characterized by the pathological accumulation of extracellular matrix (ECM) proteins. Type VI collagen alpha3 (Col6a3) is a biomarker of hepatic fibrosis, and its cleaved form, endotrophin (ETP), plays a critical role in adipose tissue dysfunction, insulin resistance, and breast cancer development. Here, we studied the effects of the Col6a3-derived peptide ETP on the progression of chronic liver diseases, such as NASH and liver cancer. We used a doxycycline (Dox)-inducible liver-specific ETP-overexpressing mouse model on a NAFLD-prone (liver-specific SREBP1a transgenic) background. For this, we evaluated the consequences of local ETP expression in the liver and its effect on hepatic inflammation, fibrosis, and insulin resistance. Accumulation of ETP in the liver induced hepatic inflammation and the development of fibrosis with associated insulin resistance. Surprisingly, ETP overexpression also led to the emergence of liver cancer within 10 months in the SREBP1a transgenic background. Our data revealed that ETP can act as a “second hit” during the progression of NAFLD and can play an important role in the development of NASH and hepatocellular carcinoma (HCC). These observations firmly link elevated levels of ETP to chronic liver disease.


Viruses ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 1767
Author(s):  
Alessandra Bartoli ◽  
Filippo Gabrielli ◽  
Andrea Tassi ◽  
Carmela Cursaro ◽  
Ambra Pinelli ◽  
...  

The hepatitis B virus is responsible for most of the chronic liver disease and liver cancer worldwide. As actual therapeutic strategies have had little success in eradicating the virus from hepatocytes, and as lifelong treatment is often required, new drugs targeting the various phases of the hepatitis B virus (HBV) lifecycle are currently under investigation. In this review, we provide an overview of potential future treatments for HBV.


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