Assessment of nutritional status and in vivo immune responses in alcoholic liver disease

1983 ◽  
Vol 38 (6) ◽  
pp. 849-859 ◽  
Author(s):  
P R Mills ◽  
A Shenkin ◽  
R S Anthony ◽  
A S McLelland ◽  
A N Main ◽  
...  
2001 ◽  
Vol 120 (5) ◽  
pp. A116-A116
Author(s):  
H SCHLEMMER ◽  
T SAWATZKI ◽  
I DORNACHER ◽  
S SAMMET ◽  
M HELLENSCHMIDT ◽  
...  

Author(s):  
Ye Rin Choi ◽  
Hyeong Seop Kim ◽  
Sang Jun Yoon ◽  
Na Young Lee ◽  
Haripriya Gupta ◽  
...  

Malnutrition and cognitive dysfunction are typical features of alcoholic liver disease (ALD) and are correlated with the development of complications. The aim of this study is to explore the effect of nutritional state and diet on cognitive function in ALD. A total of 43 patients with compensated alcoholic cirrhosis were enrolled, and neuropsychological test was assessed according to body mass index (BMI, <22 and ≥22). In the ALD animal study, mice were divided into 5 groups (n=9/group; normal liquid, 5% EtOH+regular liquid, 5% EtOH+high-carbohydrate liquid, 5% EtOH+high-fat liquid, and 5% EtOH+high-protein liquid diet) and fed the same calories for 8-week. To assess cognitive function, we performed T-maze studies weekly before/after alcohol binging. In cognitive function (BMI <22 /≥22), language score of Korea mini-mental state (7.4±1.4/7.9±0.4), Rey-complex figure (72.0±25.9/58.4±33.6), Boston naming (11.7±2.7/13.0±1.8), forward digit span (6.7±1.8/7.5±1.6), Korean Color Word Stroop (24.2±26.5/43.6±32.4), and interference score (33.9±31.9/52.3±33.9) revealed significant differences. In the T-maze test, alcohol significantly delayed the time to reach food, and binge drinking provided a temporary recovery in cognition. The alcohol-induced delay was significantly reduced in the high-carbohydrate and high-fat diet groups. Synaptic function exhibited no changes in all groups. Cognitive dysfunction is affected by nutritional status and diet in ALD.


2001 ◽  
Vol 120 (5) ◽  
pp. A116
Author(s):  
Heinz-Peter Schlemmer ◽  
Tanja Sawatzki ◽  
Ines Dornacher ◽  
Steffen Sammet ◽  
Michael Hellenschmidt ◽  
...  

Alcohol ◽  
2021 ◽  
Vol 96 ◽  
pp. 104
Author(s):  
P.T. Nagesh ◽  
R. Joshi ◽  
A.R. Amigo ◽  
Y. Zhuang ◽  
Y. Cho ◽  
...  

1986 ◽  
Vol 80 (4) ◽  
pp. 361-368 ◽  
Author(s):  
Fabrizio Spinozzi ◽  
Roberto Guerciolini ◽  
Roberto Gerli ◽  
Ivano Gernini ◽  
Francesco Rondoni ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Shashi Bala ◽  
Gyongyi Szabo

Alcoholic liver disease (ALD) is a major global health problem. Chronic alcohol use results in inflammation and fatty liver, and in some cases, it leads to fibrosis and cirrhosis or hepatocellular carcinoma. Increased proinflammatory cytokines, particularly TNF alpha, play a central role in the pathogenesis of ALD. TNF alpha is tightly regulated at transcriptional and posttranscriptional levels. Recently, microRNAs (miRNAs) have been shown to modulate gene functions. The role of miRNAs in ALD is getting attention, and recent studies suggest that alcohol modulates miRNAs. Recently, we showed that alcohol induces miR-155 expression both in vitro (RAW 264.7 macrophage) and in vivo (Kupffer cells, KCs of alcohol-fed mice). Induction of miR-155 contributed to increased TNF alpha production and to the sensitization of KCs to produce more TNF alpha in response to LPS. In this paper, we summarize the current knowledge of miRNAs in ALD and also report increased expression of miR-155 and miR-132 in the total liver as well as in isolated hepatocytes and KCs of alcohol-fed mice. Our novel finding of the alcohol-induced increase of miRNAs in hepatocytes and KCs after alcohol feeding provides further insight into the evolving knowledge regarding the role of miRNAs in ALD.


2001 ◽  
Vol 34 ◽  
pp. 203
Author(s):  
I. Dornacher ◽  
T. Sawatzki ◽  
S. Sammet ◽  
M. Hellenschmidt ◽  
P. Bachert ◽  
...  

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