Digestive Diseases and Sciences

, Volume 58, Issue 10, pp 2840–2849 | Cite as

The Role of Food for the Formation and Prevention of Gastrointestinal Lesions Induced by Aspirin in Cats

  • Hiroshi Satoh
  • Kikuko Amagase
  • Koji Takeuchi
Original Article



The effects of feeding conditions (fasted or fed) and dietary fiber (DF) in the diet on gastrointestinal (GI) damage induced by aspirin (ASA) were examined in cats.


Plain ASA (P-ASA, 20 mg/kg) or one enteric-coated ASA tablet (EC-ASA, containing 100 mg ASA) was administered p.o. once daily for 3 or 7 days just after morning meal, 3 h after the evening meal, or in the morning without a morning meal (fasted). Several types of diet, dry food (DRY, DF: 2.8 %), canned food (CAN, DF: 0.4 %), and diets with added cellulose or pectin were provided twice daily.


P-ASA or EC-ASA administered just after feeding of DRY caused marked lesions in the GI tract, although EC-ASA did not produce any lesions in the stomach. GI damage was markedly decreased when ASA was administered 3 h after the evening meal. The induction of lesions by EC-ASA was markedly decreased in cats that ate CAN, but lesions were induced in cats fed CAN with added cellulose (6 %). The addition of pectin (6 %) to the DRY markedly decreased the induction of lesions by EC-ASA.


The results indicate that the induction of GI lesions by ASA was highly dependent on the feeding conditions and DF. To minimize the induction of GI damage, it would be better to take ASA 3 h after the evening meal, or after consuming diets that contain low amounts of insoluble DF and high amounts of soluble DF.


Aspirin Enteric-coated aspirin Gastrointestinal ulcer Dietary fiber Food Cat 



The authors are greatly indebted to Tomoaki Fukumoto, Ami Yokoi and Taiki Kawabata, Students in Kyoto Pharmaceutical University, Kyoto, Japan for their technical collaboration, and to Dr. Satomi Ebara, Department of Anatomy, Meiji University of Integrative Medicine, Kyoto, Japan for valuable advice on histological studies.

Conflict of interest



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Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  1. 1.Division of Pathological Sciences, Department of Pharmacology and Experimental TherapeuticsKyoto Pharmaceutical UniversityKyotoJapan

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