HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ronis, M. J. J. Articles by Badger, T. M. Search for Related Content PubMed PubMed Citation Articles by Ronis, M. J. J. Articles by Badger, T. M.

---

ORIGINAL RESEARCH ARTICLE

Alcoholic Liver Disease in Rats Fed Ethanol as Part of Oral or Intragastric Low-Carbohydrate Liquid Diets

Martin J. J. Ronis^*,1, Reza Hakkak, Sohelia Korourian, Emanuele Albano^¶, Seokjoo Yoon^||, Magnus Ingelman-Sundberg^||, Kai O. Lindros^# and Thomas M. Badger

^* Department of Pharmacology and Toxicology and Department of Physiology, UAMS, Arkansas Children’s Nutrition Center, and Department of Pediatrics, and Department of Pathology, University of Arkansas for Medical Sciences, Little Rock Arkansas, 72205; ^¶ Department of Medical Sciences, University "A. Avogadro" of East Piedmont, Novara, Italy; ^|| Division of Molecular Toxicology, Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden; and ^# National Public Health Institute, Helsinki, Finland

To whom requests for reprints should be addressed at ¹ Arkansas Children’s Nutrition Center, Slot 512-20B, UAMS, 1120 Marshall St., Little Rock, AR 72202. E-mail: RonisMartinJ{at}uams.edu

The intragastric administration of ethanol as part of a low-carbohydrate diet results in alcohol hepatotoxicity. We aimed to investigate whether comparable liver injury can be achieved by oral diet intake. Male Sprague-Dawley rats were fed ethanol as part of low-carbohydrate diets for 36–42 days either intragastrically or orally. Liver pathology, blood ethanol concentration, serum alanine amino transferase (ALT), endotoxin level, hepatic CYP2E1 induction, and cytokine profiles were assessed. Both oral and intragastric low-carbohydrate ethanol diets resulted in marked steatosis with additional inflammation and necrosis accompanied by significantly increased serum ALT, high levels of CYP2E1 expression, and production of auto-antibodies against malondialdehyde and hydroxyethyl free radical protein adducts. However, cytokine profiles differed substantially between the groups, with significantly lower mRNA expression of the anti-inflammatory cytokine interleukin 4 observed in rats fed low-carbohydrate diets orally. Inflammation and necrosis were significantly greater in rats receiving low-carbohydrate alcohol diets intragastrically than orally. This was associated with a significant increase in liver tumor necrosis factor and interleukin 1ß gene expression in the intragastric model. Thus, oral low-carbohydrate diets produce more ethanol-induced liver pathology than oral high-carbohydrate diets, but hepatotoxicity is more severe when a low-carbohydrate diet plus ethanol is infused intragastrically and is accompanied by significant increases in levels of proinflammatory cytokines.

Key Words: ethanol • hepatoxicity • low carbohydrate • rats • oral diets • total enteral nutrition

This article has been cited by other articles:

				M. A. Gyamfi, M. G. Kocsis, L. He, G. Dai, A. J. Mendy, and Y.-J. Y. Wan The Role of Retinoid X Receptor {alpha} in Regulating Alcohol Metabolism J. Pharmacol. Exp. Ther., October 1, 2006; 319(1): 360 - 368. [Abstract] [Full Text] [PDF]

				I. BYKOV, M. PALMEN, L. PIIRAINEN, and K. O. LINDROS ORAL CHRONIC ETHANOL ADMINISTRATION TO RODENTS BY AGAR GEL DIET Alcohol Alcohol., November 1, 2004; 39(6): 499 - 502. [Abstract] [Full Text] [PDF]