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ARS Home » Southeast Area » Little Rock, Arkansas » Microbiome and Metabolism Research Unit » Research » Publications at this Location » Publication #200226
Title: Cytokine and Chemokine Expression Associated with Steatohepatitis and Hepatocyte Proliferation in Rats Fed Ethanol Via Total Enteral Nutrition

Author
item RONIS, MARTIN
item BUTURA, ANGELICA
item KOROURIAN, SOHEILA
item SHANKAR, KARTIK
item SIMPSON, PIPPA
item BADEAUX, JAMIE
item ALBANO, EMANUELE
item INGELMAN-SUNDBERG, MAGNUS
item BADGER, THOMAS

Submitted to: Experimental Biology and Medicine
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/14/2007
Publication Date: 3/3/2008
Citation: Ronis, M.J., Butura, A., Korourian, S., Shankar, K., Simpson, P., Badeaux, J., Albano, E., Ingelman-Sundberg, M., Badger, T.M. 2008. Cytokine and chemokine expression associated with steatohepatitis and hepatocyte proliferation in rats fed ethanol via total enteral nutrition. Experimental Biology and Medicine. 233(3):344-355.

Interpretive Summary: One major health outcome in obesity is liver disease, such as steatohepatitis. There are many similarities between obesity-related and alcohol-related liver diseases. Both progress from benign and reversible fat accumulation to more serious inflammation and fibrosis. It is not known why only some people (overweight/obese or alcohol consumers) develop these conditions, while others do not. One factor that seems to be important, however, is the diet. Low carbohydrate diets have been reported to result in steatohepatitis (fat accumulation + inflammation in the liver). The current study was a comprehensive analysis of the time course of alcohol-induced liver disease in rats fed alcohol and low carbohydrate diets. We found that fat accumulation, increases in ethanol metabolism, and changes in liver cells that promote disease occur very early following alcohol consumption; whereas, the appearance of inflammation, oxidative stress, liver cell death, and tissue repair occur only after more chronic ethanol consumption. These data suggest when consumed with a low carbohydrate diet, alcohol stimulates liver factors (called cytokines and chemokines) that promote progression of alcoholic liver disease. Since a relatively large percentage of Americans consume alcohol on a regular basis, more research into the relationship of dietary factors, nutritional status, physical activity indices, and alcohol is required.

Technical Abstract: One major health outcome in obesity is liver disease, such as steatohepatitis. There are many similarities between obesity-related and alcohol-related liver diseases. Both progress from benign and reversible fat accumulation to more serious inflammation and fibrosis. It is not known why only some people (overweight/obese or alcohol consumers) develop these conditions, while others do not. One factor that seems to be important, however, is the diet. Low carbohydrate diets have been reported to result in steatohepatitis (fat accumulation + inflammation in the liver). The current study was a comprehensive analysis of the time course of alcohol-induced liver disease in rats fed alcohol and low carbohydrate diets. We found that fat accumulation, increases in ethanol metabolism, and changes in liver cells that promote disease occur very early following alcohol consumption; whereas, the appearance of inflammation, oxidative stress, liver cell death, and tissue repair occur only after more chronic ethanol consumption. These data suggest when consumed with a low carbohydrate diet, alcohol stimulates liver factors (called cytokines and chemokines) that promote progression of alcoholic liver disease. Since a relatively large percentage of Americans consume alcohol on a regular basis, more research into the relationship of dietary factors, nutritional status, physical activity indices, and alcohol is required.