What is the pathogenesis of liver damage induced by ethanol?

They investigated the effects of ethanol on the IGF-I system with the involvement of JNK1/2 activity and ADH by using each chemical inhibitor in primary cultured rat hepatocytes. The results indicate that ethanol inducedp-JNK1/2 activation is associated with the IGF-I system and cell viability in hepatocytes. Furthermore, alcohol dehydrogenase is involved in the relationship between ethanol-induced inactivation of p-JNK1/2 and the changes of the IGF-I system and cell viability.

Body of text: Insulin-like growth factor (IGF)-I is a peptide that plays an important role in regulating metabolism, growth, and differentiation. Although the relationships between ethanol-induced cellular action and apoptosis via MAPK including JNK1/2 activity have been reported previously, the secretory mechanism by which the IGF-I system (IGF-I secretion, IGF-I mRNA expression, and IGF-IR activity) remains to be elucidated in primary cultured hepatocytes.

A research article to be published on January 28, 2008 in the World Journal of Gastroenterology addresses this question. Using Radioimmunoassay, RT-PCR, MTT assay, and Westernblotting, the authors investigates the relationship of IGF-I system and JNK1/2 as well as ADH activity by adding specific JNK1/2 and ADH inhibitor during ethanol exposure.

Their main findings are: (1) ethanol transiently increased p-JNK1/2 activity at 60 min and then decreased it at 180 min. (2) ethanol-induced transient activation of p-JNK1/2 increased in the IGF-I system, but this decreased when p-JNK1/2 was inactivated. Furthermore, IGF-IR activity also regulates ethanol-induced secretion and synthesis of IGF. (3) Cell viability is decreased via ADH by ethanol. These findings might be helpful to understand the pathogenesis of liver damage induced by ethanol, and may lead to a rational therapeutic intervention against ethanol toxicity.

Reference: Oh YI, Kim JH, Kang CW. Effects of ethanol on insulin-like growth factor- I system in primary cultured rat hepatocytes: Implications of JNK1/2 and alcoholdehydrogenase. World J Gastroenterol 2008; 14(27): 4324-4331
http://www.wjgnet.com/1007-9327/14/4324.asp

Correspondence to: Chang-Won Kang, MD, PhD, Department of Veterinary Physiology, College of Veterinary Medicine, Bio-Safety Research Institute, Chonbuk National University, Jeonju 561-756, Korea. cwkang@chonbuk.ac.kr
Telephone: +82-63-2703715 Fax: +82-63-2703780

World Journal of Gastroenterology (WJG), a leading international journal in gastroenterology and hepatology, has established a reputation for publishing first class research on esophageal cancer, gastric cancer, liver cancer, viral hepatitis, colorectal cancer, and H pylori infection and provides a forum for both clinicians and scientists. WJG has been indexed and abstracted in Current Contents/Clinical Medicine, Science Citation Index Expanded (also known as SciSearch) and Journal Citation Reports/Science Edition, Index Medicus, MEDLINE and PubMed, Chemical Abstracts, EMBASE/Excerpta Medica, Abstracts Journals, Nature Clinical Practice Gastroenterology and Hepatology, CAB Abstracts and Global Health. ISI JCR 2003-2000 IF: 3.318, 2.532, 1.445 and 0.993. WJG is a weekly journal published by WJG Press. The publication dates are the 7th, 14th, 21st, and 28th day of every month. WJG is supported by The National Natural Science Foundation of China, No. 30224801 and No. 30424812, and was founded with the name of China National Journal of New Gastroenterology on October 1, 1995, and renamed WJG on January 25, 1998.

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